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Flashcards in INBR 7 - Neurobiology Deck (100):
1

1 Kondensasi dan Fragmentasi kromatin, dilatasi dan blebbing dari dinding inti, dan pengeriputan sel.

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

 

 

(A)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

2

2 Memobilisasikan sistem kekebalan A. Apoptosis B. Nekrosis C. Apoptrosis dan Nekrosis D. Bukan A, B dan C

(B) ;Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

3

3 Mekanisme kematian sel setelah terapi radiasi

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(C)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

4

4 Jenis kematian sel dideteksi dengan pemeriksaan anneksin V/propidium iodida .

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(C)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

5

5 Strategi-strategi farmakologi yang menghambat kaspase 8 bisa menurunkan bentuk kematian sel semacam ini.

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(A)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

6

6 Lisis sel terjadi cepat

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(B)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

7

7 Translokasi posfatidil-serin ke membran eksternal plasma luar merupakan karakteristik awal model kematian sel ini

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(A)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

8

8 Pembentukan tangga DNA pada ‘gel electrophoresis’.

A. Apoptosis

B. Nekrosis

C. Apoptrosis dan Nekrosis

D. Bukan A, B dan C

(A)

Cellular injury, including DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis. Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products known as caspases. Two major pathways of caspase-dependent apoptosis have been identified. One pathway is initiated by the formation of a death-inducing cell surface receptor signaling complex (e.g. , Fas), leading to aggregation and activation of caspase 8. A second pathway is triggered by intracellular stress, such as DNA damage, and is primarily associated with the activation of caspase 9. During this latter pathway, signals received by the mitochondria (e.g. , after DNA injury) stimulate the release of a variety of proapoptotic molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a multiprotein complex composed of APAF- 1 , caspase 9, cytochrome c, and ATP. This, in turn, leads to activation of caspase 9 via allosteric regulation by APAF- 1 . Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases, such as 3 and 7, by cleavage. These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apoptotic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response) . Necrosis, o n the other hand, results in rapid cell lysis and a widespread inflammatory reaction without the activation of internal cell death pathways. Sometimes it is referred to as "extrinsic cell death ," as opposed to apoptosis, which is the result of endogenous cell death pathways. A characteristic biochemical feature of apoptosis is DNA fragmentation into multiple smaller fragments, which are readily detected by agarose gel electrophoresis as a characteristic "DNA ladder" formation. In contrast, necrosis causes random cleavage of DNA, resulting in a diffuse smear on DNA electrophoresis. The annexin V (A V)/propidium iodide (PI) assay appears to be the most sensitive, specific, and user-friendly method for measuring apoptosis but also concurrently provides quantitative data about the number of vital and necrotic cells. In the early stages of apoptosis, phosphatidyl serine (PS) is externalized to the outer plasma membrane. Fluorescein isothiocvanate (FITC)-labeled AV, in the presence of calcium ions, immediately adheres to PS, which results in green fluorescence of the cells. This binding serves as a specific indicator of early-stage apoptosis in cells whose cell membrane is still intact, as demonstrated by the exclusion of the nuclear stain propidium iodide. (PI ) . In cells that have lost their membrane integrity (necrotic cells), P I readily traverses the leaky membrane and binds to the DNA, inducing red fluorescence of the nucleus. The AV/PI assay can, therefore, not only measure the extent of early apoptosis (Av+;pr-) but also concurrently provides information about the number of vital cells (Av-;pi-) and necrotic cells (AV+/PI+) . Of note, differentiating between necrotic (AV+fPI+) and late apopfotic (AV+fPI+) cells may be difficult with this assay. The terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) method also measures cellular apoptosis (the method traditionally used), but it has proven to be less specific and sensitive and more time-consuming and expensive than the AV/PI assay, as described in the literature ( Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross, pp. 41-44; Schwartz, p p . 1268-12 79) .

9

9 Ion channel manakah yang bertanggung jawab untuk membawa aliran listrik dalam fase repolarisasi pada sel-sel rambut koklear ?

A. Saluran NA+

B. Saluran Ca2+

C. Saluran Ca2+ -saluran K+ sensitif

D. Saluran Cll-

E. Saluran Mg2+

(C).

The origin of electrical resonance during hearing has been determined by recording isolated hair cells using voltage-clamp techniques. A positive deflection of the hair bundle or injection of current into the cell with a microelectrode allows W influx into the cell and depolarization. Depolarization opens voltage-sensitive C a2+ channels , which augments depolarization by allowing Ca2+ entry into the cell. As C a2+ accumulates in the cytoplasm, it activates Ca2+sensitive rz+ channels, which along with voltage-sensitive K+ channels allow for K+ efflux and repolarization of hair cells ( Kandel, pp. 620-622 ) .

10

10. Manakah diantara penyebab-penyebab di bawah ini yang menambah rigiditas deserebrasi ?

A. Pemotongan radiks dorsalis

B. Inaktivasi kimiawi nukleus vestibularis lateralis

C. Pemotongan γ n motor neuron

D. Aktivasi formasio retikular modula

E. Merusak lobe flokulonodularis dari serebelum

(E)

Decerebrate rigidity occurs following isolation o f the brainstem from more rostral regions of the brain. This was demonstrated in animals that underwent surgical transection between the superior and inferior colliculi, which resulted in hyperreflexia and increased extensor tone due to loss of descending inhibitory tracts. Transection results in disruption of at least three key descending pathways. First, the lateral vestibular nucleus and pontine reticular formation are released from the inhibitory control of the cerebral cortex, which facilitates extensor motor neurons of the anns and legs. Second, projections from the red nucleus to the spinal cord are disrupted; these normally inhibit extensor motor neurons of the arms and legs. And last, the medullary reticular formation, which also inhibits extensor tone, is 9 / 10 Intensive Neurosurgery Board Review inoperative because of the loss of excitatory input from the cerebral cortex. The net effect is profound facilitation of extensor motor neurons of the arms and legs by the lateral vestibular nuclei and pontine reticular formation. Destruction of the vestibulocerebellum (flocculonodular lobe) also increases contraction of tonic extensors by releasing the lateral vestibular nucleus from tonic inhibition, which facilitates extensor motor neurons of the anns and legs. Sectioning the dorsal roots, chemically inactivating the lateral vestibular nucleus, acute injury in the thoracic spine, and sectioning of the y motor neurons all decrease decerebrate rigidity. Patients with significant brain injury above the level of the red nucleus (or at its rostral margin) exhibit a postural state called decorticate rigidity, characterized by contraction of extensors in the l egs and flexors of the arms. One reason for this is that the rubrospinal tract in humans projects only as far as the cervical spine, which may counteract vestibulospinal facilitation of arm extensors but not leg extensors ( Kandel, p p . 654-656, 717, 841; Green berg, pp. 118-119; Pritchard, pp. 254-259; Merritt, p. 18) .

11

11. Pelepasan neurotransmitter pada terminal sinaptik terutama dipicu oleh ion?

A. Na+

B. K+

C. Cl-

D. Ca2+

E. Mg2+

(D) The quanta] release of neurotransmitter by synaptic vesicles occurs by a specialized method of exocytosis at the active zones of the presynaptic terminal requiring calcium. Synaptic vesicles are bound to cytoskeletal elements near the active zone by synapsins. With depolarization, calcium/ calmodulin-dependent protein kinase phosphorylates these synapsin proteins, resulting in the release of the synaptic vesicle (Kandel, pp. 262-2 7 4 ) .

12

12. Manakah yang akan menyebabkan hiperpolarisasi atas neuron yg istirahat (resting neuron)

A. Kenaikan konduktan Cl-

B. Kenaikan konduktan Na+

C. Kenaikan konduktan Ca2+

D. Penurunan konduktan K+

E. Kenaikan konduktan K+

12. E.

A typical neuron has a resting membrane potential of -65 m V. The equilibrium potential for K+ is -86 m V, and an increase in conductance of this ion would result in movement of the neurons membrane potential toward -86 mV and hyperpolarization. The E(;1 ( -66 m V) is very similar to the resting membrane potential of a neuron (-65 mV), and an increase in conductance of this anion would not result in any drastic change in the resting membrane potential of a cell. Increasing Na+ and ea2+ conductance would lead to depolarization of the neuron instead of hyperpolarization• ( Ka ndel, p p . 150-170)

13

13. Manakah diantara hal-hal yang berikut ini yang akan meningkatkan kecepatan konduksi axon?

1. Menaikkan diameter axon

2. Menaikkan resistensi trans-membran (Rm)

3. Menurunkan kapasitansi membran (Cm)

4. Menurunkan konstanta panjang membran (α)

13. A.

How rapidly an action potential travels through an axon depends on a number of factors, including the internal resistance of an axon (RJ; the transmembrane resistance of the plasma membrane (R,n), (inversely related to the number of ion channels), and membrane capacitance (em). To better understand the relationship between these properties, we can use the analogy of a leaky straw. There are two paths that the water can take: one, down the inside of the straw, and the other, through the leaky holes along the straw. How much water flows along each of these paths depends on the relative resistance of each of these pathways, as most of the water will tend to go down the path of least resistance. The same principles apply to current flowing down an axon. The current can either continue to flow down the axon or exit the axon through a leaky plasma membrane (ion channels). Increasing the diameter of the axon will decrease the R, and allow the action potential to be conducted down the axon with increased conduction velocity. Increasing the Rm by myelination facilitates flow down the axon as well, just as wrapping tape around a leaky straw would also facilitate water flow down the inside of the straw. The ratio of Rm to R, is called the membrane length constant (A) and represents the distance between the point of peak depolarization produced by Na+ influx and the point where the depolarization has declined to approximately 3 7% of peak value. A indicates that Na+ current is more likely to spread further along the axon if the membrane resistance is higher than the cytoplasmic resistance (increasing A) . I n terms of em, this property indicates how well the plasma membrane can hold positive and negative charges. Thinner membranes generally hold charges better than thicker ones because the electrostatic attraction between ions on opposite sides of the plasma membrane increases with decreased membrane thiclmess. Therefore thinner axons with increased membrane capacitance have decreased conduction velocity because it takes more time for current traveling clown an axon to change the electrical potential of the adjacent membrane (and continue current propagation clown the axon). The addition of myelin around an axon increases conduction velocity because it decreases em (increases membrane thickness). Decreasing the relative refractory period does not affect conduction velocity, but decreasing the diameter of the

14

14. Manakah pernyataan di bawah ini yang benar untuk utrikulus dan sakulus ?

A. Dengan kepala pada posisi tegak, orientasi utrikulus yaitu vertikal pada dinding medial dari vestibulum

B. Utrikulus dan sakulus merespon akselerasi angular.

C. Di dalam makula utrikulus, sel-sel rambut tersusun dengan orientasi kinosilium menjauh dari striola

D. Permukaan makula memanjang ke dalam membran labirin dan terendam dalam perilim

E. Ujung sel-sel rambut ditutup oleh membran otolitik, yang mana dilekati kristal kalsium karbonat (otokonia).

14. E.

Refer to Figure 1 . 14A. The utricle and saccule are located in the vestibule, a large chamber that separates the semicircular canals and the cochlea. The sensory epithelia of the saccule and utricle are called the maculae. Each macula consists of numerous hair cells surrounded by supporting cells resting on a connective tissue base. The orderly arrangement of hair cells within the macula gives the appearance of a curved equatorial line called the striola. In the utricle, the hair cells are arranged with the kinocilium oriented toward the striola, whereas in the saccule, the hair cells are polarized away from the striola. This anatomic polarity ensures that the two otolith organs can respond to linear acceleration or head tilt in any direction. The surface of the macula extends into the membranous labyrinth, which is bathed in endolymph, not perilymph. The macular surface is covered with a gelatinous structure, the otolithic membrane, which has calcium carbonate crystals (otoliths or otoconia) embeclclecl on its surface. Relative movement between the otolithic membrane - and the surface of hair cells is the essential macular stimulus, since this produces movement (bending) of hair cells, which results in ionic current flow at the base of hair cells and neurotransmitter release. With the head in a neutral position, the macula of the utricle lies in the horizontal plane (on the floor of the vestibule) and the macula of the saccule lies in the vertical plane (on the medial wall of the vestibule) . Linear acceleration is detected by the maculae, whereas angular acceleration is detected by the specialized hair cells of the semicircular canals, called the cristae ampullaris ( Ka ndel , pp. 802-814; Pritchard, pp. 250-253)

A image thumb
15

Tn. X, 52 tahun menjalani reseksi subtotal glioblastoma multiforme yang berasal dari lobus fronalis kanan dan meluas ke nukleus didalam dari hemisfir tersebut. Pasca-operasi, dia menjalani terapi radiasi pada otak secara keseluruhan, dan menerima 1, 3-bis-2¬kloroetil-1-nitrourea (BCNU), Delapan bulan kemudian pasien yang bersangkutan terkena proses penyakit ini kembali. 15. Resistensi tumor ini terhadap BCNU kemungkinan disebabkan oleh:

A. Konsentrasi tinggi O6-alkilguanin-DNA alkil-transferase (O6-AGAT) pada sel-sel tumor.

B. Tumor ini berada dalam S-fase dari siklus sel (fase resistensi) pada waktu pemberian BCNU

C. Sel-sel tumor ini tidak memiliki topoisomerase II, yang menyebabkan strand DNA transien pecah selama induksi kemoterapi.

D. Sel-sel tumor ini tidak memiliki protein permukaan sel yang mengenal BCNU

E. Obat yang mengganggu sawar darah¬otak yang tidak diberikan bersamaan dengan pemberian BCNU

A

The nitrosoureas (BCNU, CCNU) are alkylating agents and are the most widely used drugs for patients with malignant brain tumors. They alkylate DNA in multiple locations, primarily on guanine but also on adenine and cytosine. The resultant DNA cross links often produce single- or doublestranded DNA breaks and eventual tumor cell death. 06- AGAT is a repair enzyme that mediates repair of alkylation products of nitrosoureas. It has been noted that approximately 70% of tumors have high levels of 06-AGAT and are often resistant to nitrosourea chemotherapy ( Bernstein, p p . 231-232)

16

n. X, 52 tahun menjalani reseksi subtotal glioblastoma multiforme yang berasal dari lobus fronalis kanan dan meluas ke nukleus didalam dari hemisfir tersebut. Pasca-operasi, dia menjalani terapi radiasi pada otak secara keseluruhan, dan menerima 1, 3-bis-2¬kloroetil-1-nitrourea (BCNU), Delapan bulan kemudian pasien yang bersangkutan terkena proses penyakit ini kembali. 16. Bahan manakah yang memiliki potensi menaikkan tingkat respons terhadap kemoterapi BCNU? A. Irinotecan (CPT-11) B. Tamoxifen C. Suramin D. O6-benzylguanine E. 1-(2-kloroetil)=3=sikloetil-1-nitrosourea (OCNU)

D Attempts t o modify resistance t o nitrosoureas are ongoing. As stated in the previous discussion (question 1 5), 06-AGAT mediates the repair of alkylating products of nitrosoureas. I nhibition of this repair protein has been the subject of a number of clinical trials using 06-benzylguanine, a methylating agent. Tamoxifen inhibits protein kinase C, CPT- 1 1 is a topoisomerase I inhibitor, and suramip works by inhibiting growth factors (FGF, I GF-1 , PDGF) . These agents do not modify resistance to alkylating agents. The addition of CCNU can potentially increase the risk of nitrosoureainduced side effects ( Bernstein, pp. 229-332 )

17

17. Penelitian eksperimental dengan menggunakan pendekatan transfer gen bunuh diri HSV-tk/GCV pada berbagai model binatang membuktikan adanya regresi tumor dan survival memanjang meskipuh efisiensi transduksi kurang dari 10 persen. Keberhasilan mengaplikasikan dengan terapi gen bunuh diri kanker (suicide gene cancer theraphy) pada penelitian ini, terlepas dari tidak tuntasnya pengiriman vektor genetika ke semua sel tumor, kemungkinan disebabkan oleh:

A. Transfer GCV posforilase (pGCV) ke dalam sel-sel tumor yang tidak tertransdusi melalui gap junctions.

B. Reaksi inflamasi yang disebabkan vektor virus, mengakibatkan aktifnya proses pengiriman sinyal kematian pada sel (Fas/APO-1)

C. Regulasi-ke atas dari p53 yang serta merta menyebabkan pelepasan mediator-mediator apoptotis (misalnya kaspase 8) dari mitokondria

D. Regulasi-ke atas dari cAMP, pembawa pesan kedua yang telah dipastikan dapat menghentikan proliferasi pada fase G1 siklus sel.

E. Transfer vektor-vektor biral ke dalam sel sel tumor non-transduksi melalui lubang-lubang berselaput klatrin.

A

The mechanism \\•hereby untransd1,1ced tumor cells die during gene therapy is called the "bystander effect." Until recently, this mechanism was poorly understood; it requires the presence of gap junctions that allow the transfer of toxic metabolites into untransduced tumor cells. In the I-ISVtk/ GCV approach, the nucleoside analogue GCV becomes cytotoxic after being converted to its triphosphorylated form by HSV-tk and host cellular kinases. It acts as a chain terminator and interrupts DNA synthesis in replicating cells. Phosphorylated GCV can then be transported into surrounding untransduced cells via gap junctions and induce cell death. The degree of bystander effect in individual tumors depends on the cell type and its capability to express gap junctions, the vector used, and the enzymatic activity of the therapeutic gene. The other choices have not been sho\\'11 to propagate toxicity from transduced to untransduced cells (Bernste i n , pp. 280-281).

18

18. Apa yang menjadi satu-satunya neurotransmitter yang disintesis dalam vesikel sinaptik?

A. Dopamin

B. Norepineprin

C. Asetilkolin

D. Serotonin

E. Senyawa P

B

Acetylcholine (Ach) is synthesized from cholin and acetyl-CoA by the enzyme choline acetyltransferas::c ACh is utilized by spinal cord motor neurons at the neurc.muscular junction, all preganglionic autonomic neu postganglionic parasympathetic neurons, postganglioni s:- pathetic neurons to sweat glands, and within the basalis of Meynert. ACh is metabolized in the synaptic "by acetylcholinesterase into acetate and choline. then recycled b y reuptake into the terminal bourreceptor-mediated endocytosis. Dopamine epinephrine (NE), and epinephrine are all synthesized he same precursor molecule, the amino acid L-cyr Tyrosine hydroxylase synthesizes L-DOPA from r:-r " - = and is the rate-limiting enzyme for both DA and :sis. Aromatic amino acid decarboxylase then symhesizrom L-DOPA. Dopamine is synthesized by neuronssubstantia nigra and arcuate nucleus of the hyporh ' and is also active in some mesolimbic and me tracts. Reserpine prevents the uptake of DA into vesicles. Dopamine ex-hydroxylase is located on rh brane of synaptic vesicles, where it converts DA w synaptic vesicle itself. NE is the only neurotransmme synthesized within the synaptic v'esicle. NE exerrs feedback on tyrosine hydroxylase. NE is the neurmra:ter of most postganglionic sympathetic neurons and - 12 I ntensive Neurosurgery Board Review found in the locus ceruleus. After NE is released into the synaptic cleft, the termination of its bioactivity is primarily accomplished by reuptake into the presynaptic neuron. NE reuptake is blocked by cocaine. NE is also metabolized by catechol 0-methyltransferase (COMT) and monoamine oxidase (MAO) in the cytoplasm of numerous cells. The medications tropolone and selegiline inhibit the enzymes COMT and :tvfA08, respectively. Serotonin (an indole) is synthesized from the amino acid tryptophan. Tryptophan is initially converted into 5-hydroxytryptophan by the enzyme tryptophan hydroxylase, which represents the rate-limiting step. Then 5-hydroxytryptophan is converted into serotonin by the enzyme 5-hydroxytryptophan decarboxylase. Serotonergic neurons are primarily found in the raphe nuclei of the brainstem reticular formation. Serotonin reuptake is inhibited by several antidepressants, including the selective serotonin reuptake inhibitors (SSRis; e.g. , fluoxetine) and the tricyclic antidepressants ( Kandel, p p . 280-295; Pritchard, pp. 32-45)

19

19. Paling peka terhadap peregangan kulit

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

D

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

20

20. Terutama peka terhadap getaran (600stimuli/detik) 

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

C

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

21

21. Hampir semuanya ditemukan sebagi klusterdi pusat sulkus papilaris.

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

E

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

22

22. Memberikan sensasi paling tajam untuk kesan ruang.

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

E

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

23

23. Membatasi saluran pencernaan. A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

A

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

24

24. Serat-serat aferen pada refleks peregangan.

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

E

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

25

25. Memindahkan Informasi mengenai tekanan dan tekstur.

A. Ujung-ujung saraf bebas

B.Korpuskel MEISSNER

C. Korpuskel PACINIAN

D. Korpuskel RUFFINI

E. Diskus MERKEL

F. Bukan salah satu diatas

E

Sensory endings of the skin can be classified on a structural basis i n to encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel's discs, and hair follicle receptors. Encapsulated endings include Meissner's corpuscles, pacinian corpuscles, and Ruffini's corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract and are found between epitheli al cells of the skin, in the cornea, and in a variety of connective tissues including the dermis, fascia, ligaments, joint capsules, periosteum, and muscle. They are either myelinated or unmyelinated, and most detect pain; however, some detect crude touch, pressure, and tickling sensations. Merkel's discs are found i n hairless regions of the body including the fingertips. They terminate in the deeper aspects of the epidermis, are slowly adapting, and transmit information about pressure and texture. l'vlerkel's disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the skin. 1vleissner's corpuscles also provide sharp resolution of spatial patterns, but the image is generally not as sharp as the one produced by l'l'lerkel's endings because they have slightly larger receptive fields. lvierkel's discs are normally found in clusters at the center of the papillary ridge. Hair-follicle receptors ll'ind around hair follicles adjacent to a sebaceous gland. Some surround the hair follicle and others run parallel to it. These receptors are rapidly adapting and respond to the bending of hair follicles. Encapsulated receptors include lv leissner's corpuscles, pacinian corpuscles, and Ruffini corpuscles. Jvleissner's corpuscles are located in the dermal papillae of the skin, especially in the palms and soles of the feet. They are oval in shape and consist of a stack of flattened Schwann cells arranged transversely along their long axis. They are very sensitive to touch (especially stroking, fluttering), are rapidly adapting, and allo\1' people to distinguish between two pointed structures placed together on the skin. Pacinian corpuscles are very similar physiologically to Meissner's corpuscles, are widely distributed, and are numerous in the dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 1 00-500 J.. l!n across (largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve enters the corpuscle, loses the myelin sheath, and then passes through the central core before terminating i n an expanded fashion. Pacinian corpuscles are rapidly adapting and sensitive mainly to vibration. Ruffini's corpuscle is located in the dermis of hairy areas, is a slowly adapting mechanoreceptor, and responds mainly when the skin is stretched. Muscle spindles and group Ia fibers i nnervate the afferent limb of the stretch reflex ( Kandel, p p . 430-450, 565).

26

26. Struktur manakah yang dinilai melalui manuver doll’s eye?

A. Traktus vestibulospinalis lateralis

B. Traktus vestibulospinalis medialis

C. Saraf vestibular

D. Serebelum

E. Korteks serebri

C The doll's eye test assesses the integrity of the vestibula-ocular reflexes, which include the vestibular labyrinths, vestibular nerves bilaterally, vestibular nuclei, and motor nuclei of the cranial nerves involved with eye movements (nen•es III, IV, and VI). The doll's eye maneuver does not test the integrity of the cerebral cortex, cerebellum, or medial and lateral vestibulospinal tracts, as they are n o t part o f the vestibulo-ocular circuit. T h e vestibula-ocular reflex stabilizes the eyes during head movements in order to keep an image focused on the retina. Rotation of the head to the right initiates compensatory eye movements to the left as a result of endolymph in the right semicircular canal flowing to the left ( toll'ard the utricle). As the endolymph flows through the ampulla, the cupula and underlying stereocilia bend toward the utricle. The resultant depolarization of the receptors causes an increase in the firing of the vestibular nerve, which reaches the vestibular nuclei, which, in turn, project to the motor nuclei of the extraocular muscles. The endolymph in the left (opposite) semicircular canal flows away from the utricle, causing hyperpolarization of hair cells and a lower firing rate of cranial nerves and vestibular nuclei on that side ( Kandel, p p . 802-809)

27

27. Di antara pernyataan-pernyataan mengenai photo-transduksi di dalam retina di bawah ini, pernyataan manakah yang paling benar?

A. Kerucut lebih baik daripada batang pada hampir semua tugas visual, kecuali deteksi cahaya redup di malam hari

B. Adanya cahaya menyebabkan terbukanya saluran-saluran sodium channels di dalam photoreceptor dari retina.

C. Aliran sodium ke dalam sel-sel photoreseptor dimungkinkani oleh cAMP channels.

D. Di kegelapan, hiperpolarisasi sel-sel photoreseptor dari retina disebabkan oleh keluarnya natrium intrasel.

E. Metarhodopsin II, produk pemecahan dari rhodopsin, mengakibatkan deaktivasi molekul posfodiesterase.

A

The absorption of light by the photoreceptor cells of the retina results in a cascade of e\'ents (three distinct stages) that leads to a change in ionic fluxes across the plasma membrane of these cells. In rod cells, the visual pigment rhodopsin has two parts. The protein portion, opsin, is embedded in the disc membrane and does not absorb light, whereas the light-absorbing portion, retinal (derivative of vitamin A), can assume several different isomeric conformations, two of which absorb light. In the nonactivated form, rhodopsin contains the 1 1-cis isomer of retinal, which fits into the opsin binding site. In response to light, the 1 1-ci.s isomer changes to the all-tra11s configuration of rhodopsin, which no longer fits inside the opsin binding site . The opsin then undergoes a conformational change to semistable metarhodopsin II, which triggers the second stage of phototransduction. In this stage, metarhodopsin II activates a large number of phosphodiesterase molecules via an intermediate molecule termed transducin. Transducin, in turn, catalyzes the hydrolysis of cGMP molecules, which are required by cG!IlP channels for sodium conduction into the cell. This results in less cGMP, and the closure of cGMP-dependent sodium channels (stage 3 of the phototransduction cycle) . The light-evoked closing of these channels results in less inward sodium current and, therefore, hyperpolarization of the cell. In the absence of light, cGMP is no longer broken clown, sodium channels are reope.necl, and the cell becomes depolarized again. Cones perform better than rods in all visual tasks except the detection of dim light at night. Conemediated vision has higher acuity than rod-mediated vision, provides better resolution of images, and mediates color vision ( Kandel, p p . 508-514)

28

28. Gap junctions akan tertutup sebagai respons terhadap :

A. Berkurangnya konsentrasi Ca2+ intraselular.

B. Bertambanaya konsentrasi K+ ekstraselular

C. Kenaikan konsentrasi proton di dalam sel.

D. Bertambahnya konsentrasi Ca2+ ekstraselular

E. Gap junctions, berbeda dari ion channels, tetap terbuka terus menerus.

C Gap junctions are sensiti\'e to different modulating factors that control their opening and closing in different tissues. For instance, most gap junctions close in response to lowered cytoplasmic pH or eleYated cytoplasmic Ca2+. These two properties se1Ye to decouple damaged cells from other cells, since damaged cells have ele,•atecl levels of Ca2+ and protons (lower pH). Neurotransmitters released from other cells can also modulate the opening and closing of gap junctions ( Kandel, pp. 178-180 )

29

29. Neuron unipolar terutama mempersarafi struktur apa?

A. Sistem saraf simpatis

B. Sekresi kelenjar eksokrin dan kontraksi otot polos

C. Sel-sel otot jantung (nodus AV)

D. Sekresi kelenjar adrenal dan glomerulus renal

E. Kontraktilitas otot usus halus dan usus besar

B

Unipolar neurons are the simplest in morphology. They ha\'e no dendrites and a single axon, which gives rise to multiple processes at the terminal. In humans, they control  exocrine gland secretions and smooth muscle contractility (Martin, p. 2 )

30

30. Di antara pernyataan-pertanyaan mengenai koklea di bawah ini, pernyataan manakah yang paling benar?

A. Nada frekuensi tinggi menyebabkan membran basilar bergetar secara maksimal pada apeks nya

B. Sel-sel rambut dari koklea biasanya tidakberadaptasi terhadap kekuatan stimuli, kecuali jika dipicu oleh nada frekuensi rendah

C. Potensi endokoklear + 40mV ada diantara perilimf dengan endolimf

D. Defleksi stereosilia pada kedua arah dapat menyebabkan depolarisasi.

E. Sel-sel rambut membentuk sinap kimia dengan sel bipolar dari ganglion spiralis

E

The hair cells of the cochlea form chemical synapses with bipolar cells of the spiral ganglion. Although the precise neurotransmitter released remains unclear, studies in animyls show that transmitter release by hair cells is evoked by/presynaptic depolarization and requires the presence of Ca2+, as in most other synapses. The neurotransmitter involved is believed to be glutamate. The cochlea is a fluid-filled tube coiled 2 1/z times around itself to resemble a snail shell. Reissner's membrane and the basilar membrane separate the cochlea into three chambers, the scala vestibule (SV), scala tympani (ST), and scala media (SM), which contains the organ of Corti. The SV and ST are filled with perilymph, which resembles CSF, and are continuous with one another at the helicotrema, a small opening located at the apex of the cochlear coil. The SM is filled IYich endolymph, a clear liquid with high K+ concentration formed by the stria vascularis. Pressure waves resulting from sound cause the basilar membrane to move up and down, "•hi h results in a shearing movement of hair cells against the Le - torial membrane. It is the physical bending of the hair cells toward the scala vestibuli that causes them to depolarize (Kchannels and voltage-sensitive Ca2+ channels) . Movemem ir. the opposite direction causes hyperpolarization (Ca2+-sensiu,-rz+ channels) (see discussion for question 9). The difieren; regions of the basilar membrane are sensitive to differem ir - quencies of sound. High frequencies cause the membrane 14 Intensive Neurosurgery Board Review to vibrate maximally at its base, whereas low frequencies cause maximal vibration near the apex. There is a marked difference in ion concentrations between the perilymph of the SV and the endolymph of the SM, which produces an endocochlear potential of +80 m V. Hair cells do adjust to sustained stimuli by a process of adaptation (to either highor low-frequency sounds), which manifests itself as a progressive decrement in receptor potential during protracted hair-bundle deflection (Pritchard, pp. 229

31

31. Pernyataan tentang reseptor olfaktoris manakah yang benar?

A. Reseptor olfaktoris pada awalnya menayangkan adaptasi yang cepat

B. Umur sel-sel reseptor olfaktoris yaitu sekitar 9 bulan.

C. Satu sel reseptor olfaktoris biasanya memberi respons hanya pada satu odoran.

D. Potensial reseptor terjadi manakala Na+ channels tertutup dengan cara mirip foto transduksi.

E. Kesemuanya diatur oleh cGMP

A Olfactory receptors (ORs) display rapid adaptation initially and little afterwards . Within the olfactory system, an olfactory stimulus results in the opening of sodium channels, which leads to depolarization and action potentials. These action potentials can increase in frequency to about 20/s. Adenylate cyclase activity catalyzes the formation of cAMP, resulting in opening of many additional channels, which can also increase the rate of discharge in olfactory neurons. Each olfactory neuron is capable of responding to many different odorants, as determined by electrophysiologic studies. The life span of ORs varies from 30 to 120 days in mammalian species. Replacement cells are delivered by mitosis of basal cells. The relatively rapid turnover of ORs makes them partially susceptible to damage after radiation therapy and/or chemotherapeutic agents, which target rapidly dividing cells ( Kandel, p p . 626-636; Pritchard, p p . 266-267).

32

32. Sistem sensoris manakah yg mengirimkan sinyal baik ke talamus maupun ke korteks serebri ?

A. Diskriminasi dua-titik

B. Pengecap

C. Penghidu

D. Nyeri

E. Keseimbangan

C Taste and sensation from the head are carried to the ventroposterior medial (VP!II) nucleus of the thalamus. Sensation and proprioception from the body reach the ventroposterior lateral (VPL) nucleus of the thalamus. The visual system utilizes the lateral geniculate nucleus (LGN) and the auditory system the medial geniculate nucleus (MGN) prior to being relayed to the cortex. Some olfactory information bypasses the thalamus to reach the orbitofrontal cortex, but it should be noted that some projections subserving smell can reach the orbitofrontal cortex via the mediodorsal (MD) thalamic nucleus. The olfactory system, therefore, relies on parallel processing to transmit olfactory inputs to the cortex (Kandel, p. 633)

33

33. Sel-sel paling sensitif terhadap terapi radiasi

Q image thumb

C/B

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

34

34. Kekurangan gizi atau berdesak-desakkan merupakan kondisi yang mendorong sel bergerak ke dalam fase siklus sel ini

Q image thumb

E

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

35

35. Sel-sel dapat menggabungkan thimidin anallog ke dalam inti DNA

Q image thumb

A

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

36

36. Sel-sel yang paling resisten terhadap terapi radiasi

Q image thumb

A

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

37

37. P15 dan P16 dapat menyebabkan pertumbuhan berhenti di dalam fase siklus sel ini

Q image thumb

D

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

38

38. TP53-dependent growth arrest yang mengikuti kerusakan DNA terjadi dalam fase ini

Q image thumb

D Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

39

39. Fase yang paling variabel dari siklus sel dalam hal durasinya

Q image thumb

D

Cells are most sensitive to radiation during the G2 and M phases of the cell cycle and most resistant in the late S phase. G 1 cells have intermediate sensitivity. The precise mechanism(s) accounting for these variations remains unclear, but studies have shown that differences in a cell's ability to repair DNA damage in different phases after radiation may play an important part. In the G1 phase of the cycle, the nucleus has a diploid amount of DNA (2C), which increases to 4C by the end of the S phase. Only cells in the S phase (DNA synthetic phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle; such cells can eventually re-enter the cell cycle at a later point in time. Mitosis is the most easily identifiable stage of the cell cycle by light microscopy. The genes encoding p 1 6 (CDKN2A) a n d p 1 5 (CDI

40

40. Berapa resting membrane potential untuk sel-sel saraf?

A. -100mV

B. -90mV

C. -80mV

D. -65mV

E. -40mV

D

In resting nerve cells the resting membrane potential is

41

41. Berapa konsentrasi ion Ca2+ ekstraseluler pada otak?

A. 0,7mM/l

B. 2 mM/L

C. 125mM/L

D. 150 mM/L

E. Jawaban A, B, C dan D semuanya salah

B

Neurons maintain a high concentration of K+ ions and organic anions inside the cell, and ions such as Na+, Cl-, and Ca2+ are more highly concentrated outside of the cell ( Ka ndel, pp. 125-139) . 

A image thumb
42

42. Kolom neuron pada daerah 3a dari korteks somato-sensoris menerima input terutama dari reseptor tipe apa ?

1. Reseptor kulit beradaptasi cepat (Rapidly adapting skin receptors)

2. Reseptor kulit beradaptasi cepat dan lambat. (Slowly and Rapidly adapting skin receptors)

3. Reseptor tekan dan posisi sendi (Pressure and joint position receptors)

4. Reseptor regangan otot (Muscle stretch receptors)

D ( Kandel, pp. 456-459)

A image thumb
43

43. Manakah yang paling benar dari potensial aksi (action potential)? 1. Potensial aksi dimediasi keseluruhannya oleh perubahan pada K+ voltage-gated channels 2. Tingkat fluktuasi influk Na+ mulai melamban begitu potensi membran mendekati EK+ 3. Ambang untuk awal aksii potensial biasanya sekitar +15mV 4. Fase menurun dari aksi potensial dimediasi oleh hambatan aktivasi pada konduktansi K+

D. The rising phase of an action potential is due to a stimulus that results in the activation of voltage-gated Na+ channels. The rate of Na+ influx begins to slow as the membrane reaches the membrane potential for Na+ (not W), resulting in a peak amplitude when the Na+ channels become inactivated. The decline in the action potential is then mediated by the delayed activation of voltage-gated K+ channels. The efflux of K+ ions is greatest at the peak of the action potential and begins to decline as the membrane potential approaches the equilibrium potential for I

44

44. Sel dengan lapang reseptif konsentris sepanjang jalur visual ditemukan di lokasi sebagai berikut: A. Retina B. Retina dan saraf optik C. Retina dan nukleus genikulatum laterale D. Retina, nukleus genikulatum laterale, lapisan 4 dari korteks visual E. Hanya sel-sel pada korteks premotorik saja

C. Both ganglion cells in the retina and the lateral geniculate nucleus are known to have both "on-center" and "off-surround," or concentric, receptive fields . Cells in the optic nerve and premotor cortex are not known to possess such characteristics. Simple cells in layer IV of the visual cortex do not have circular receptive fields but instead respond to stimuli as lines and bars (rectangles) ( Ka ndel , p p . 517-522 , 528-529)

45

45. Apa neurotransmitter utama dari sel Renshaw? A. Glisin B. Asetilkolin C. GABA D. Serotinin E. Glutamat

A. A special class of inhibitory interneurons called Renshaw cells are found in laminae VII and VIII of the spinal cord. These cells have muscarinic cholinergic receptors that receive a-motor-neuron cholinergic colla.teral projections. The Renshaw cell then exerts a negative feedback on the a motor neuron and other homonymous a motor neurons, called recurrent inhibition. The neurotransmitter released by Renshaw cells is glycine. Renshaw cells also make inhibitory synaptic connections with Ia inhibitory interneurons; this arrangement regulates reciprocal inhibition of antagonistic motor neurons. Renshaw cells receive input from several descending pathways in the spinal cord (Carpenter, p p . 57-79; Kandel, pp. 720-721).

46

46. Pasien dengan homonimous hemianopsia akibat lesi parietal akan menujukkan defisiensi gerakan mata _______ dari lesi, mengakibatkan optikokinetik nistagmus. Optikokinetik nistagmus ini akan berkurang bila bola mata berputar _________ sisi dari lesi. A. Berlawanan dari sisi, ke arah B. Ke arah sisi tersebut, menjauh dari C. Berlawanan dari sisi, menjauh dari D. Ke arah sisi, ke arah E. Jawaban A, B, C dan D semuanya salah

D. The precise pathways of the opticokinetic system remain unclear but are believed to be similar to smooth pursuits. The pathway is believed to extend from the visual association areas (I8 and 19) to the horizontal gaze center of the abducens nucleus in the pons. The pathway from the left visual association area is believed to terminate in the left pontine gaze center, resulting in pursuit movement of the eyes to the left. Similarly, the right \'isual association region produces movements to the right. A patient with a pure occipital lobe lesion theoretically should have no difficulty with pursuits, since the pathways originate in more anterior regions. The opticokinetic response should, therefore, be symmetric. A patient with homonymous hemianopsia and a parietal lesion will have deficient pursuit movements to the same side of the lesion, resulting in an asymmetric opticokinetic response (OI

47

47. Semua fitur biokimia di bawah ini yang berhubungan dengan reseptor neurotransmitter kimiawi adalah benar, KECUALI: A. Reseptor-reseptor ini kemungkinan merupakan membrane-spanning protein B. Reseptor-reseptor ini dapat bekerja secara langsung atau tidak langsung untuk mempengaruhi response sinaptik C. Reseptor-reseptor ini dapat mempengaruhi sel dengan mengaktivasi pembawa pesan kedua(second messenger), seperti cAMP atau diasilgliserol D. Reseptor-reseptor ini dapat membantu memperkuat jalur yang terlibat dalam pembelajaran E. Tempat pengikatan pada reseptor nikotinik asetilkolin biasanya mencakup, sub-unit α maupun β

E. Direct receptors like nicotinic ACh receptors are also referred to as ionotropic receptors, which gate ionic currem rapidly over only a few milliseconds. The ACh receptor itself is a transmembrane protein composed of fiye subuni (a2

48

48. Semua pernyataan dibawah ini yang berhubungan kanalis semi-sirkularis adalah benar, KECUALI: A. Pergerakan endolimf dalam masing-masing kanal berlawanan dengan arah perputaran kepala. B. Signal dari serabut aferent primer tidak brenti setelah putaran kepala berhenti. C. Akselerasi linier dari kepala cukup untuk mengaktifkan kanalis semisirkularis posterior. D. Dasar ampulla mengandung bangunan spesifik dari sel-sel rambut yang ditutupi oleh suatu lapisan gelatin yang dinamakan kupula E. Sel-sel rambut pada kanalis horisontalis berpolarisasi ke arah utrikulus, dan yang ada di kanalis semisirkularis anterior dan posterior berpolarisasi menjauhi utrikulus.

C. Refer to Figure 1 .48A. One end of each semicircular canal contains an enlarged region known as the ampulla, where the flow of endolymph serves as a mechanical stimulus for sensory transduction. The floor of the ampulla contains specialized hair cells, the crista ampullaris, and is covered by a gelatinous layer known as the cupula. The stereocilia of the hair cells insert into the cupula. These hair cells are stimulated by changes in endolymph circulation induced by head rotation. The movement of endolymph within each canal is opposite to the direction of head rotation . The response in each pair of semicircular canals (one on each side of the head) is opposite as well. Rotation of the head or angular acceleration is sufficient to stimulate a response in the semicircular canals but insufficient to stimulate the macula of the utricle, which requires linear acceleration. Firing typically ceases once head movement stops. Hair cells in the horizontal canal are polarized toward the utricle, and those in the anterior and posterior semicircular canals are polarized away from the utricle ( Kandel , pp. 802-806; Pritchard, pp. 2 50-253)

A image thumb
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49. Transmisi sinaptik lambat antara nosiseptor dan neuron kornu dorsalis dimediasi terutama oleh neurotransmitter apa ?: A. Substansi P B. Glutamat C. Asetilkolin D. ATP E. Serotonin (A) 50. Motor unit terdiri dari A. Satu kelompok α motor neuron menuju otot tertentu B. Satu kelompok α dan γ motor neuron menuju otot tertentu C. Satu kelompok α motor neuron menuju otot tertentu dan semua serabut otot yang dipersarafinya D. Satu kelompok serabut otot yang dipersarafi oleh satu motor neuron E. Semua kelompok otot yang dipersarafi oleh radiks ventralis

A. Slow-excitatory synaptic transmission between nociceptors and dorsal horn neurons in the marginal layer of lamina I and substantia gelatinosa of lamina II is mediated primarily by substance P , released by A8 and C fibers (Kand e l , pp. 477-479).

50

50. Motor unit terdiri dari A. Satu kelompok α motor neuron menuju otot tertentu B. Satu kelompok α dan γ motor neuron menuju otot tertentu C. Satu kelompok α motor neuron menuju otot tertentu dan semua serabut otot yang dipersarafinya D. Satu kelompok serabut otot yang dipersarafi oleh satu motor neuron E. Semua kelompok otot yang dipersarafi oleh radiks ventralis

D. The motor unit is the functional unit of muscle contraction; it includes a single motor neuron and all of the muscle fibers it innervates ( Kandel , p . 81)

51

51. Serat sensoris 1b dari otot paling peka terhadap modalitas sensoris yang mana : 1. Panjang otot 2. Tekanan kuat 3. Kecepatan perubahan dalam panjang 4. Regangan otot

D . Refer to Table 1

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52

52. Manakah di antara komponen di bawah ini yang merupakan komponen ‘muscle spindle’: 1. Serat otot intrafusal 2. Ujung annulospiral 3. Ujung flower-spray 4. Serabut γ motor

E. Sensory fibers from muscle are typically classified according to their diameter. Group Ia sensory fibers (annulospiral endings and flower-spray endings) are between 12 to 20 Jlm in diameter, myelinated, sensitive to muscle length and rate of change in length, and receive their input from muscle spindles. Group lb fibers are similar in diameter to group la, are also myelinated, and are most sensitive to muscle tension from Golgi tendon organs. Group II sensory fibers receive their input from secondary spindle endings and nonspindle endings and are between 6 to 12 Jlm in diameter. Secondary spindle endings are sensitive to muscle length and nonspindle endings are sensitive to deep pressure. Group III sensory fibers receive input from free nerve endings, are between 2 to 6 Jlm in diameter, and are responsive to pain as well as chemical and temperature stimuli. Type IV sensory endings are similar to type III with the exception of being smaller in diameter (0 . 5 to 2 Jlm). Intrafusal fibers of muscles spindles are i n parallel with extrafusal muscle fibers, whereas Golgi tendon organs (GTOs) are connected in series to skeletal muscle fibers, innervated by lb sensory afferents, and sensitive to muscle tension, as described above ( Kandel, pp. 720-723). 52. E. Refer to Figure 1 .

A image thumb
53

53. Dengan memukul ligamen patellae dengan menggunakan palu refleks akan menyebabkan aktivasi struktur sebagai berikut: 1. Ujung-ujung annulospiral 2. Ujung-ujung flower-spray 3. neuron motorik α 4. Muskulus kuadrisep

A. Muscle spindles are the sensory receptors of skeletal muscle that signal changes in muscle length. Changes in muscle length are closely associated with changes in the angles of the joints that the muscles cross; thus muscle spindles are capable of sensing relative positions of various body segments. The main components of the muscle spindle include intrafusal muscle fibers with noncontractile central regions, afferent sensory endings originating from the center of the intrafusal fibers (flowerspray and annulospiral nerve endings) , and efferent motor fibers (static and dynamic y motor neurons) ( Kandel, pp. 7 18- 719).

54

54. Diantara pernyataan-pernyataan mengenai neuron di bawah ini, manakah yang benar: A. Neuron Golgi tipe I membentuk jaras serabut saraf pendek pada otak dan medula spinalis B. Neuron Golgi tipe II memiliki axons panjang yang berahir di sekeliling badan sel C. Neuron Golgi Tipe I bersifat inhibisi D. Volume sitoplasma dalam badan sel selalu melebihi yang ditemukan dalam neurite E. Jumlah neuron Golgi Tipe II jauh melebihi neuron tipe I

E. Golgi type I axons are typically long and include the pyramidal cells of the cerebral cortex, the Purkinje cells of the cerebellar cortex, and the motor cells of the spinal cord. Golgi type l l neurons have shorter axons, greatly outnumber type I neurons, and are usually inhibitory. They have short dendrites, which gives them a star-shaped appearance. The volume of cytoplasm in the axons and dendrites usually exceeds the volume in the cell body (Bear, p. 41; Carpenter, pp. 65, 126, 2 14 , 229, 233, 330, 390, 395).

55

55. Transport Retrograde A. Kinesin B. Dynein C. Dynamin D. Bukan A, B atau C E. Semua A, B dan C

B. Membranous organelles and secretory vesicles are transported to the axon terminal via fast anterograde axonal transport. This mode of transport is dependent on the protein kinesin and ATP and occurs at a rate of > 400 mm/day. IUnesin binds the organelle or vesicle and then forms intermittent cross bridges with tracks of microtubules, resulting in stepwise transport down the axon. The pharmacologic agents vinblastine and colchicine bind to and interfere with microtubule structure (not kinesin) , thereby disrupting fast anterograde transport. There are several types of slow anterograde axonal transport. Component A utilizes a protein called dynamin, is GTPdependent, and facilitates transport of cytosolic proteins and cytoskeletal elements. It is much slower than fast anterograde transport, occurring at a rate of 0.2 to 2 . 5 mm/day. Component B is slightly faster, at 2 to 4 mm/day, and utilizes an actin/myosin motor complex in the transport of cytosolic proteins, actin, and spectrin. Fast retrograde axonal transport occurs at a rate of > 400 mm/day and is dependent on the protein dynein and hydrolysis of ATP. Retrograde transport facilitates the passage of endosomes from the axon terminal to the neuron soma. Endosomes contain various proteins (such as ner>e growth factor) and even pathogens (such as rabies \•irus or tetanus toxin) that are taken up by the axon terminal \•ia endocytosis (Kandel, pp. 99-103 )

56

56. Transport Anterograde cepat A. Kinesin B. Dynein C. Dynamin D. Bukan A, B atau C E. Semua A, B dan C

A. Membranous organelles and secretory vesicles are transported to the axon terminal via fast anterograde axonal transport. This mode of transport is dependent on the protein kinesin and ATP and occurs at a rate of > 400 mm/day. IUnesin binds the organelle or vesicle and then forms intermittent cross bridges with tracks of microtubules, resulting in stepwise transport down the axon. The pharmacologic agents vinblastine and colchicine bind to and interfere with microtubule structure (not kinesin) , thereby disrupting fast anterograde transport. There are several types of slow anterograde axonal transport. Component A utilizes a protein called dynamin, is GTPdependent, and facilitates transport of cytosolic proteins and cytoskeletal elements. It is much slower than fast anterograde transport, occurring at a rate of 0.2 to 2 . 5 mm/day. Component B is slightly faster, at 2 to 4 mm/day, and utilizes an actin/myosin motor complex in the transport of cytosolic proteins, actin, and spectrin. Fast retrograde axonal transport occurs at a rate of > 400 mm/day and is dependent on the protein dynein and hydrolysis of ATP. Retrograde transport facilitates the passage of endosomes from the axon terminal to the neuron soma. Endosomes contain various proteins (such as ner>e growth factor) and even pathogens (such as rabies \•irus or tetanus toxin) that are taken up by the axon terminal \•ia endocytosis (Kandel, pp. 99-103 )

57

57. Transport Anterograde lambat A. Kinesin B. Dynein C. Dynamin D. Bukan A, B atau C E. Semua A, B dan C

C. Membranous organelles and secretory vesicles are transported to the axon terminal via fast anterograde axonal transport. This mode of transport is dependent on the protein kinesin and ATP and occurs at a rate of > 400 mm/day. IUnesin binds the organelle or vesicle and then forms intermittent cross bridges with tracks of microtubules, resulting in stepwise transport down the axon. The pharmacologic agents vinblastine and colchicine bind to and interfere with microtubule structure (not kinesin) , thereby disrupting fast anterograde transport. There are several types of slow anterograde axonal transport. Component A utilizes a protein called dynamin, is GTPdependent, and facilitates transport of cytosolic proteins and cytoskeletal elements. It is much slower than fast anterograde transport, occurring at a rate of 0.2 to 2 . 5 mm/day. Component B is slightly faster, at 2 to 4 mm/day, and utilizes an actin/myosin motor complex in the transport of cytosolic proteins, actin, and spectrin. Fast retrograde axonal transport occurs at a rate of > 400 mm/day and is dependent on the protein dynein and hydrolysis of ATP. Retrograde transport facilitates the passage of endosomes from the axon terminal to the neuron soma. Endosomes contain various proteins (such as ner>e growth factor) and even pathogens (such as rabies \•irus or tetanus toxin) that are taken up by the axon terminal \•ia endocytosis (Kandel, pp. 99-103 )

58

58. GTP-Dependent A. Kinesin B. Dynein C. Dynamin D. Bukan A, B atau C E. Semua A, B dan C

C. Membranous organelles and secretory vesicles are transported to the axon terminal via fast anterograde axonal transport. This mode of transport is dependent on the protein kinesin and ATP and occurs at a rate of > 400 mm/day. IUnesin binds the organelle or vesicle and then forms intermittent cross bridges with tracks of microtubules, resulting in stepwise transport down the axon. The pharmacologic agents vinblastine and colchicine bind to and interfere with microtubule structure (not kinesin) , thereby disrupting fast anterograde transport. There are several types of slow anterograde axonal transport. Component A utilizes a protein called dynamin, is GTPdependent, and facilitates transport of cytosolic proteins and cytoskeletal elements. It is much slower than fast anterograde transport, occurring at a rate of 0.2 to 2 . 5 mm/day. Component B is slightly faster, at 2 to 4 mm/day, and utilizes an actin/myosin motor complex in the transport of cytosolic proteins, actin, and spectrin. Fast retrograde axonal transport occurs at a rate of > 400 mm/day and is dependent on the protein dynein and hydrolysis of ATP. Retrograde transport facilitates the passage of endosomes from the axon terminal to the neuron soma. Endosomes contain various proteins (such as ner>e growth factor) and even pathogens (such as rabies \•irus or tetanus toxin) that are taken up by the axon terminal \•ia endocytosis (Kandel, pp. 99-103 )

59

59. Mengikat vinblastine dan colchicines untuk A. Kinesin B. Dynein C. Dynamin D. Bukan A, B atau C E. Semua A, B dan C

D.Membranous organelles and secretory vesicles are transported to the axon terminal via fast anterograde axonal transport. This mode of transport is dependent on the protein kinesin and ATP and occurs at a rate of > 400 mm/day. IUnesin binds the organelle or vesicle and then forms intermittent cross bridges with tracks of microtubules, resulting in stepwise transport down the axon. The pharmacologic agents vinblastine and colchicine bind to and interfere with microtubule structure (not kinesin) , thereby disrupting fast anterograde transport. There are several types of slow anterograde axonal transport. Component A utilizes a protein called dynamin, is GTPdependent, and facilitates transport of cytosolic proteins and cytoskeletal elements. It is much slower than fast anterograde transport, occurring at a rate of 0.2 to 2 . 5 mm/day. Component B is slightly faster, at 2 to 4 mm/day, and utilizes an actin/myosin motor complex in the transport of cytosolic proteins, actin, and spectrin. Fast retrograde axonal transport occurs at a rate of > 400 mm/day and is dependent on the protein dynein and hydrolysis of ATP. Retrograde transport facilitates the passage of endosomes from the axon terminal to the neuron soma. Endosomes contain various proteins (such as ner>e growth factor) and even pathogens (such as rabies \•irus or tetanus toxin) that are taken up by the axon terminal \•ia endocytosis (Kandel, pp. 99-103 )

60

60. Seluruh pernyataan mengenai GABA-responsive channels di bawah ini adalah benar, KECUALI: A. GABA-A, reseptor terdiri dari lima sub unit (α2β2γ) B. Pikrotoksin menghambat reseptor GABA-A, setelah terikat pada sub-unit β C. Reseptor GABA-b meningkatkan konduktanis K+ dan menghambat potensial post-sinaptik (IPSP) setelah mengikat baklofen D. Sub-unit β dari reseptor GABA-A mengikat benzodiazepine E. Pengikatan alkohol, barbiturate, atau benzodiazepine ke reseptor GABA-A, meningkatkan konduktansi Cl-

. D. GABA A receptors consist of five subunits: two a .. and one y subunit. All three subunits bind while the a and subunits bind barbiturates and the y subunit binds benzodiazepines. After binding GABA, the channel 18 Intensive Neurosurgery Board Review opens and permits the entry of Ct into the cell, generating an inhibitory postsynaptic potential (IPSP). The binding of neuromodulators such as alcohol, barbiturates, and benzodiazepines increases the GABA-induced Cl- current but does not open the channel directly. Picrotoxin inhibits the GABAA receptor after binding to the

61

61. Ion mana yang memblokir pori ion reseptor N-metil-D-aspartate (NMDA) glutamate waktu potensial membran istirahat (resting membrane potential) A. CA2+ B. NA+ C. K+ D. Mg2+ E. Cl-

6 1 . D. Glutamate receptors are ionotropic channels that induce EPSPs and include the N-methyl-o-aspartate glutamate (N!vlDA) receptor, the kainate receptor, and the kainate-quisqualate (AMPA) receptor. The N1viDA receptor is an ion channel of high conductance that is permeable to Ca2+, Na+, and K+. This receptor contributes only to the later phases of the EPSP because it is active only in the presence of its ligand and membrane depolarization. This channel is unique in this regard because its activity is dependent upon a neurotransmitter and membrane potential. At resting membrane potential, Mg2• blocks the ion pore of the NMDA channel. With membrane depolarization, the Mg2• is displaced from the channel , allowing ion conduction to occur efficiently. The opening of the N1vlDA channel also requires glycine as a cofactor. The NMDA channel is inhibited by PCP and selectively blocked by APV. This channel is important in long-term potentiation at the neuronal synapse because its activity leads to an increase in cytosolic Ca2+ with subsequent activation of second messengers involved with longlasting synaptic modifications. High levels of glutamate are toxic to neurons, and this toxicity is mediated primarily by the Nl\•fDA channel. With excessive levels of glutamate, cytosolic Ca2• increases significantly, activating proteases and phospholipases that generate free radicals toxic to neurons. The non-NMDA glutamate receptors (kainate and AMPA) are permeable to Na• and W and are responsible for the generation of the early, large component of the EPSP. There are also metabotropic glutamate receptors that act through G proteins and second-messenger systems ( Kandel, p p . 2 19-221).

62

62. Menghambat pelepasan glisin A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

E Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

63

63. Mengikatkan diri kepada sub-unit α dari creseptor nikotinik A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

B Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

64

64. Melekat pada sinaptobrevin protein A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

E Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

65

65. Melekat pada t-SNARE dan v-SNARE A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

H Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

66

66. Secara selektif mengaktivasi Gs. A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

F Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

67

67. Inhibitor non-depolarisasi terhadap reseptor nikotinik kolinergik A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

C Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

68

68. Inaktivasi G1 A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

I Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

69

69. Agonis dari reseptor 5-HT1C A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

J Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

70

70. Antagonis dari reseptor 5-HT3 (Ionotropik) A. Tetrabenazine B. ɑ-bungarotoksin C. D-tubocurarine D. Strihnin E. Toksin tetanus F. Toksin Kolera G. Barbiturat H. Toksin Botulinus I. Toksin Pertusis J. LSD K. Ondansetron L. Tidak satupun dari A sampai dengan K

K . Ion channels conduct ions at extremely high rates, are selective for specific ions, and are regulated or gated. Gated ion channels can be regulated by changes in voltage, chemical transmitters (ligands) , and mechanical factors. Ligandgated channels include glutamatergic channels, cholinergic channels, glycinergic channels, and GABAergic channels. Acetylcholine-activated channels include nicotinic and muscarinic receptors. Nicotinic cholinergic receptors are ionotropic channels that are permeable to Na• and I and pertussis toxin which inactivates G,. Tetanus toxin specifically cleaves the protein synaptobrevin, while botulinus toxins cleave t-SNAREs and v-SNAREs, which subsequently results in the inhibition of synaptic vesicle release at the terminal. The docking, fusion, and release of synaptic vesicles appears to involve distinct interactions between vesicle proteins (synaptobrevin and synaptotagmin, v-SNAREs) and proteins of the nerve terminal plasma membrane (syntaxins and neurexins, tSNAREs) ( Kandel, pp. 196-200, 2 19, 241-243, 1197- 1199, 1215-1216).

71

71. Bukti klinis mengenai defisit neurologis mungkin tidak akan muncul sampai aliran  darah regional turun mencapai 50% atau di bawah ambang rata-ratanya. Pada tingkat aliran darah serebral manakah ( dalam mL/100 g/menit) edema sitotoksik berkembang dari adanya kegagalan Na+K+- ATPase?
A. 40 – 50
B. 25 – 30
C. 16 – 20
D. 10 – 12
E. < 10

(D)

A image thumb
72

72. Manakah di antara hal-hal berikut ini yang diyakini menjadi mediator vasoaktif utama yang memainkan peranan integral dalam vasomodulasi?
A. Karbon Monoksida
B. Metabolit asam arakhidonik
C. Nitro oksid
D. Adenosin
E. ATP

(C)

73

73. Sel dari neural crest menjadi asal dari bangunan di bawah ini, KECUALI:
A. Ganglia radiks ventral
B. Se post-ganglionik dari ganglion simpatis dan parasimpatis
C. Sel-sel kromaffin dari medulla adrenal
D. Melanosit
E. Sel Schwann

(A)

74

74. Manakah yang merupakan gambaran umum dari degenerasi WALLERIAN ?
1. Degenerasi dan pagositosis dari segmen aksonal distal
2. Kromatolisis (periferalisasi endoplasmic retikulum kasar disertai penambahan sintesis protein) akibat berkurangnya pengiriman secara retrograde neurotropik faktor.
3. Pembengkakan segmen proksimal akson akibat transpor anterograde di akson yang terus menerus.
4. Tingkat kematian sel neuron setelahaksotomi lebih tinggi pada post-sinaptik
sistem saraf perifer (PNS) dibandingkan pada sistem saraf pusat

(A)

75

75. Serat otot lurik

A. Serat otot merah
B. Serat Otot putih
C. Serat otot merah dan putih
D. Bukan A, B atau C

(C)

76

76. Mengandung banyak mikokondria, kontraksi dan relaksasi lambat

A. Serat otot merah
B. Serat Otot putih
C. Serat otot merah dan putih
D. Bukan A, B atau C

(A)

77

77. Kapasitas metabolisme aerobic

A. Serat otot merah
B. Serat Otot putih
C. Serat otot merah dan putih
D. Bukan A, B atau C

(C)

78

78. Mengandung banyak persediaan glikogen.

A. Serat otot merah
B. Serat Otot putih
C. Serat otot merah dan putih
D. Bukan A, B atau C

(B)

79

79. Hanya terdiri dari filament-filamen aktin. 

Q image thumb

(E)

A image thumb
80

80. Memendek selama kontraksi otot

Q image thumb

(B/E)

A image thumb
81

. Zona H 

Q image thumb

(B)

A image thumb
82

Pita A

Q image thumb

(D)

A image thumb
83

83. Diskus Z

Q image thumb

(A)

A image thumb
84

84. Seorang Konsultan neuropatologi diminta untuk menentukan usia kandungan dari janin, meski pun tampaknya telah berusia kandungan sekitar 18 minggu. Kriteria neuroanatomik manakah yang terbaik dan dapat digunakan patologis ini untuk menentukan usia kandungan janin tersebut pada sekitar kurun waktu tersebut?
A. Tingkat penutupan bumbung saraf
(neural tube) B. Pola sulci serebri
C. Kematangan mielinasi
D. Jumlah ɑ-fetoprotein pada serum ibu.
E. Ketebalan lapisan ependimal yang membatasi rongga ventricular.

(B)

85

85. Hal benar manakah dari pertanyaan di bawah nu yang berhubungan dengan cairan serebospinal (CSF)?
A. 90% disekresi oleh pleksus koroid
B. Obat anestesi yang bersifat volatile dan
CO2 meningkatkan pembentukan CSF
C. Pengeluaran CSF melalui araknoid villi bergantung pada volumenya (volume dependent)
D. Dihasilkan setiap hari sekitar 750 cc CSF
E. Norepineprin meningkatkan kecepatan produksi CSF.

(B)

86

86. Penutupan neuropor kaudal  

A. Hari 12

B. hari 14

C. Hari 16
D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(G)

A image thumb
87

. Notochord mulai tumbuh

A. Hari 12 

B. hari 14

C. Hari 16

D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

C

A image thumb
88

88. Lipatan-lipatan neuronal (neural fold) hampir menyatu

A. Hari 12

B. hari 14

C. Hari 16

D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(E)

A image thumb
89

89. Penutupan neuropor rostral

A. Hari 12
B. hari 14
C. Hari 16
D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(F)

A image thumb
90

90. Pembentukan neural groove

A. Hari 12
B. hari 14
C. Hari 16
D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(D)

A image thumb
91

91. Diskus bilaminar terbentuk 

A. Hari 12

B. hari 14
C. Hari 16
D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(B)

A image thumb
92

92. Prosensepalon terbagi menjadi telensepalon dan diensepalon  

A. Hari 12
B. hari 14
C. Hari 16
D. Hari 18
E. Hari 21
F. Hari 24
G. Hari 26
H. Bukan A sampai dengan G.

(H)

A image thumb
93

93. Neurotransmiter manakah yang berperan dalam menhasilkan potensial eksitatori pasca-sinaptik (EPSP)?
1. Asetilkolin
2. GABA
3. Glutamat
4. Glisin

(B)

A transient postsynaptic membrane depolarization
caused by presynaptic release of a neurotransmitter is called
an excitatory postsynaptic potential (EPSP). Synaptic activation
of ACh-gated and glutamate-gated ion channels causes
EPSPs. Synaptic activation of GABA-gated ion channels
(Cl-- and K•-mediated) causes an inhibitory postsynaptic
potential (IPSP) ( Kandel, pp. 207 - 2 18 ) .

94

94. Apa yang terjadi selama asidosis metabolic akut alam mempertahankan homeostatis pH dari CNS?
1. Hiperventilasi kompensatoris
2. Penurunan pCO2 dalam CSF
3. Alkalosis CSF paradoksal
4. Pleksus koroideus mengeluarkan karbonat hasil katalise oleh karbonik anhidrase

A.

Despite the absence of large quantities of protein for
buffering, CSF pH is maintained in a narrow range, even with
major changes in systemic pH. This is emphasized by the fact
that the range of CSF pH compatible with life is very narrow
( 7 . 1 9 to 7 .38) in comparison to systemic pH (6.9 to 7.8). A
number of important mechanisms are involved to achieve
this tight balance, which center around the fact that pC02
diffuses readily across the blood-brain barrier (BBB) , but
both bicarbonate and hydrogen ions are relatively impermeable.
As a result, the pH of the CSF and brain interstitium
is less effectively buffered in acute respiratory acid-base disorders
than metabolic ones. For example, acute metabolic
acidosis results in compensatory hyperventilation, an immediate
reduction in CSF pC02, and an increase in CSF pH
(paradoxical alkalosis). During respiratory acidosis, compensatory
mechanisms such as carbonic anhydrase-catal)·zed
generation of bicarbonate by the choroid plexus and deamination
of glutamic acid typically return CSF and brain interstitial
pH toward normal in a matter of hours, not minutes or
seconds (Fishman, pp. 135-136; Simmons, pp. 347-348).
95. C. There is evidence of increased growth of meningiomas

95

95. Meningioma telah terbukti berhungan dengan reseptor progesteron. Pada bagian mana dari sel tumor meningioma reseptor ini ditemukan ?
A. Endoplasmik retikulum
B. Membran sel
C. Inti Sel
D. Ribosoma
E. Kompleks golgi

C.

There is evidence of increased growth of meningiomas
during various phases of the menstrual cycle and during
pregnancy, which has sparked interest in the effects of hormone
receptors on meningiomas. Studies have shown that
meningiomas express intranuclear, functionally active progesterone
receptors, but their precise relationship to tumor
growth remains uncertain (Kaye and Laws, pp. 4 5 , 1 1 7 , 724;
Carroll et a l . , pp. 92-97 ) .

96

96. Mengikatkan diri pada reticulum endoplastis halus, menyebabkan pelepasan ion-ion CA2+.
A. Protein G
B. Protein kinase A
C. Protein kinase C
D. Posfolipase C (PLC)
E. Diagliserol (DAG)
F. Inositol Trifosfat (IP3)
G. cAMP
H. Bukan salah satu dari di atas

F

Chemical neurotransmitters
can exert their action by two major mechanisms. The
first is direct activation of transmitter-gated ion channels
CHAPTER 1 Neurobiology Answers 21
(acetylcholine-nicotinic receptor, AMPA, kainate, NMDA
glutamate channels, GABAA and glycine receptors) and the
second involves the activation of effector proteins by G
protein-coupled receptors (muscarinic receptors, metabotropic
glutamate receptors, GABAn, serotonin [ 5-I-IT]
receptors, D1 receptors, and certain norepinephrine [ a1 , a2,

97

97. Pembawa pesan kedua, yang mengaktivasi protein kinase C


A. Protein G
B. Protein kinase A
C. Protein kinase C
D. Posfolipase C (PLC)
E. Diagliserol (DAG)
F. Inositol Trifosfat (IP3)
G. cAMP
H. Bukan salah satu dari di atas

(E)

Chemical neurotransmitters
can exert their action by two major mechanisms. The
first is direct activation of transmitter-gated ion channels
CHAPTER 1 Neurobiology Answers 21
(acetylcholine-nicotinic receptor, AMPA, kainate, NMDA
glutamate channels, GABAA and glycine receptors) and the
second involves the activation of effector proteins by G
protein-coupled receptors (muscarinic receptors, metabotropic
glutamate receptors, GABAn, serotonin [ 5-I-IT]
receptors, D1 receptors, and certain norepinephrine [ a1 , a2,

98

98. Mengaktivasi protein kinase A.
A. Protein G
B. Protein kinase A
C. Protein kinase C
D. Posfolipase C (PLC)
E. Diagliserol (DAG)
F. Inositol Trifosfat (IP3)
G. cAMP
H. Bukan salah satu dari di atas

(G)

Chemical neurotransmitters
can exert their action by two major mechanisms. The
first is direct activation of transmitter-gated ion channels
CHAPTER 1 Neurobiology Answers 21
(acetylcholine-nicotinic receptor, AMPA, kainate, NMDA
glutamate channels, GABAA and glycine receptors) and the
second involves the activation of effector proteins by G
protein-coupled receptors (muscarinic receptors, metabotropic
glutamate receptors, GABAn, serotonin [ 5-I-IT]
receptors, D1 receptors, and certain norepinephrine [ a1 , a2,

99

99. Memiliki tiga sub-unit dengan nama α, β dan γ


A. Protein G
B. Protein kinase A
C. Protein kinase C
D. Posfolipase C (PLC)
E. Diagliserol (DAG)
F. Inositol Trifosfat (IP3)
G. cAMP
H. Bukan salah satu dari di atas

(A)

Chemical neurotransmitters
can exert their action by two major mechanisms. The
first is direct activation of transmitter-gated ion channels
CHAPTER 1 Neurobiology Answers 21
(acetylcholine-nicotinic receptor, AMPA, kainate, NMDA
glutamate channels, GABAA and glycine receptors) and the
second involves the activation of effector proteins by G
protein-coupled receptors (muscarinic receptors, metabotropic
glutamate receptors, GABAn, serotonin [ 5-I-IT]
receptors, D1 receptors, and certain norepinephrine [ a1 , a2,

100

100. Membelah PIP2 menjadi dua molekul yang bertindak sebagai pembawa pesan kedua
(second messengers).


A. Protein G
B. Protein kinase A
C. Protein kinase C
D. Posfolipase C (PLC)
E. Diagliserol (DAG)
F. Inositol Trifosfat (IP3)
G. cAMP
H. Bukan salah satu dari di atas

(D)

Chemical neurotransmitters
can exert their action by two major mechanisms. The
first is direct activation of transmitter-gated ion channels
CHAPTER 1 Neurobiology Answers 21
(acetylcholine-nicotinic receptor, AMPA, kainate, NMDA
glutamate channels, GABAA and glycine receptors) and the
second involves the activation of effector proteins by G
protein-coupled receptors (muscarinic receptors, metabotropic
glutamate receptors, GABAn, serotonin [ 5-I-IT]
receptors, D1 receptors, and certain norepinephrine [ a1 , a2,