Wiring the brain Flashcards
(162 cards)
1
Q
What is the estimated number of neurons in the human brain?
A
The human brain contains approximately 85 billion neurons.
2
Q
What are the three major stages of neuronal structure development?
A
- Cell proliferation
- Cell migration
- Cell differentiation
3
Q
Describe the process of cell proliferation in neuronal development
A
- Neural progenitors, known as radial glial cells, divide to give rise to neurons and astrocytes.
- Radial glial cells undergo symmetrical cell division early in development, expanding the neural progenitor population.
- Later in development, they switch to asymmetrical cell division, with one daughter cell migrating to the cortex and the other remaining in the ventricular zone for further divisions
4
Q
describe the “positions” of cell proliferation
A
- First position: A cell in the ventricular zone extends a process that reaches upward toward the pia.
- Second position: The nucleus of the cell migrates upward from the ventricular
surface toward the pial surface; the cell’s DNA is copied. - Third position: The nucleus, containing two complete copies of the genetic instructions, settles back to the ventricular surface.
- Fourth position: The cell retracts its arm from the pial surface.
- Fifth position: The cell divides in two.
5
Q
When do the majority of neocortical neurons in humans get generated, and at what rate?
A
-The majority of neocortical neurons are generated between the fifth week and the fifth month of gestation (pregnancy).
-Neurons are generated at an astonishing rate of 250,000 new neurons per minute during this period.
6
Q
What happens once a daughter cell commits to a neuronal fate in neuronal development?
A
Once a daughter cell commits to a neuronal fate, it will never divide again.
7
Q
Is there ongoing neurogenesis (generation of new neurons) in most parts of the adult brain?
A
No, in most parts of the brain, the neurons you are born with are all you will have in your lifetime.
8
Q
How is a cell’s fate determined?
A
Cell fate is determined by differences in gene expression during development, regulated by transcription factors.
9
Q
What makes one cell different from another?
A
The specific genes that generate mRNA and proteins make one cell different from another.
10
Q
What regulates gene expression in cells?
A
Gene expression is regulated by cellular proteins called transcription factors.
11
Q
How can the cleavage plane during cell division affect cell fate?
A
If transcription factors or upstream molecules regulating them are unevenly distributed within a cell, the cleavage plane during cell division can determine which factors are passed on to daughter cells, influencing their fate.
12
Q
What factors determine the ultimate fate of migrating daughter cells?
A
Factors including the age of the precursor cell, its position within the ventricular zone, and its environment at the time of division determine the ultimate fate of migrating daughter cells during cortical development.
13
Q
From where do cortical pyramidal neurons and astrocytes derive?
A
Cortical pyramidal neurons and astrocytes derive from the dorsal ventricular zone.
14
Q
From where do inhibitory interneurons and oligodendroglia derive?
A
Inhibitory interneurons and oligodendroglia derive from the ventral telencephalon.
15
Q
What is the role of the subplate in cortical development?
A
The subplate is a layer where the first cells to migrate away from the dorsal ventricular zone reside, and it eventually disappears as development proceeds.
16
Q
In what order do neurons of different cortical layers develop?
A
Neurons in cortical layers develop in the following order: subplate, layer VI, layer V, layer IV, layer III, and layer II.
17
Q
How does primate cortical development differ from rodents?
A
Primates, like humans, have an additional proliferative layer of cells called the subventricular zone, which contributes to the development of the upper layers of the cortex (layers II–III) and plays a role in corticocortical connections. This difference contributes to the complexity of the primate neocortex.
18
Q
How do many daughter cells migrate in the developing brain?
A
Many daughter cells migrate by slithering along the thin fibers emitted by radial glial cells that span the distance between the ventricular zone and the pia.
19
Q
What are the immature neurons that follow radial paths from the ventricular zone toward the surface of the brain called?
A
The immature neurons are called neural precursor cells.
20
Q
What happens when cortical assembly is complete?
A
When cortical assembly is complete, the radial glia withdraw their radial processes.
21
Q
Do all migrating neural precursor cells follow the path provided by radial glial cells?
A
No, about one-third of the neural precursor cells wander horizontally on their way to the cortex.
22
Q
Which type of neural precursor cells are among the first to migrate away from the ventricular zone?
A
The neural precursor cells destined to become subplate cells are among the first to migrate away from the ventricular zone.
23
Q
How is the cortex assembled in terms of the order of cell migration?
A
First cells to migrate take up residence in
subplate layer, which eventually disappears. The cortex is assembled inside out, with the first cells to arrive in the cortical plate becoming layer VI neurons, followed by layer V cells, layer IV cells, and so on.
24
Q
What gene mutation can disrupt the orderly process of cortex assembly?
A
Mutations in genes, such as the reelin gene, can disrupt the orderly process of cortex assembly. For example, in the reeler mutant mouse, neurons of the cortical plate are unable to pass through the subplate and pile up below it.
25
What is the process called when a cell takes on the appearance and characteristics of a neuron?
Cell differentiation.
26
What triggers cell differentiation in neural precursor cells?
Specific spatiotemporal patterns of gene expression
27
When does neuronal differentiation typically begin in the cortex?
Neuronal differentiation begins as soon as the neural precursor cells divide, with further differentiation occurring when they arrive in the cortical plate.
28
In what order do different types of brain cells, such as neurons, astrocytes, and oligodendrocytes, typically differentiate?
Neurons differentiate first, followed by astrocytes, and then oligodendrocytes.
29
What are the initial signs of neuronal differentiation in a neural precursor cell?
The appearance of neurites sprouting off the cell body.
30
Which structures in a differentiated neuron become recognizable as the axon and dendrites?
One of the neurites becomes recognizable as the axon, and the others become dendrites
31
Can neuronal differentiation occur outside of the brain environment, such as in tissue culture?
Yes, neuronal differentiation can occur even when the neural precursor cell is removed from the brain and placed in tissue culture.
32
What is responsible for the stereotypical architecture of cortical dendrites and axons in pyramidal neurons?
Intercellular signals, such as the protein semaphorin 3A, play a role in directing the growth of neurites and the formation of dendritic and axonal structures in pyramidal neurons.
33
What is the neocortex often compared to? How is the neocortex more accurately described in terms of structure?
A sheet of tissue. It's like a patchwork quilt with distinct areas stitched together.
34
How are most cortical neurons formed and positioned during development?
They are born in the ventricular zone and migrate along radial glia to their final cortical layer
35
What does the concept of a cortical "protomap" propose?
t suggests that migrating neural precursor cells are guided precisely to the cortical plate by radial glial fibers.
36
What does the radial unit hypothesis suggest about cortical neurons' birthplaces?
It suggests that neurons in an entire radial column of the cortex originate from the same ventricular zone birthplace
37
What contributes to the dramatic expansion of the human neocortex during evolution?
Differences in the duration of symmetrical cell division and an increase in the number of proliferative radial glial cells.
38
How do neural precursor cells find their final resting place in the developing neocortex?
Neurons in different regions of the cortex have distinct molecular identities, with unique transcription factors like Emx2 and Pax6. These factors create gradients along the anterior-posterior axis of the ventricular zone. Neurons with higher Pax6 levels migrate to the anterior neocortex, while those with more Emx2 head to the posterior cortex. Differences in transcription factors act as signals to guide neural precursor cells to their appropriate destinations.
39
What happens when mice are genetically engineered to produce less Emx2?
When mice produce less Emx2, there is an expansion of the anterior cortical areas like the motor cortex and a shrinkage of posterior cortical areas such as the visual cortex.
40
What is the consequence of knocking out Pax6 in mice?
Knocking out Pax6 in mice leads to an expansion of the visual cortex and a shrinkage of the frontal cortex.
41
What happened when researchers replaced the parietal cortex in newborn rats with a piece of occipital cortex?
Thalamic fibers from the VP nucleus invaded the new piece of cortex, assuming the cytoarchitecture characteristic of the rodent somatosensory cortex.
42
What did the experiment conducted by Schlaggar and O’Leary suggest about the role of the thalamus in cortical development?
It suggested that the thalamus is important for specifying the pattern of cortical areas.
43
How do subplate neurons contribute to the development of cortical areas?
Subplate neurons attract appropriate thalamic axons to different parts of the developing cortex, leading to cytoarchitectural differentiation when these axons invade the cortex.
44
What is the role of the subplate layer in the assembly of the cortical quilt during brain development?
The subplate layer of earliest born neurons appears to contain the instructions for the assembly of the cortical quilt, influencing the development of cortical areas
45
What are the three phases of pathway formation in the central nervous system (CNS)?
Pathway selection, target selection, and address selection
46
In the context of the development of the visual pathway, what does "pathway selection" refer to?
Pathway selection involves the decisions made by growing axons regarding which route to take, such as crossing over at the optic chiasm or staying on the same side.
47
What is "target selection" in pathway formation?
Target selection is the decision made by growing axons to innervate the correct thalamic nucleus, such as the lateral geniculate nucleus (LGN) in the visual pathway.
48
What is the significance of "address selection" in pathway formation?
Address selection involves ensuring that the axon reaches the correct layer of the LGN and establishes retinotopy, allowing for precise visual information processing.
49
How do neurons communicate during pathway formation?
Neurons communicate during pathway formation through direct cell–cell contact, contact with extracellular secretions, and communication via diffusible chemicals. As pathways develop, communication also occurs through action potentials and synaptic transmission.
50
What is the term for the growing tip of a neurite that identifies an appropriate path for neurite elongation?
Growth cone.
51
What are the flat sheets of membrane on the leading edge of the growth cone called?
Lamellipodia.
52
What are the thin spikes extending from the lamellipodia that constantly probe the environment called?
Filopodia.
53
What is the extracellular matrix?
Fibrous proteins deposited in the spaces between cells.
54
What type of molecules in the growing axons bind to laminin, promoting axonal elongation?
Integrins.
55
What is the mechanism that causes axons growing together to stick together?
Fasciculation.
56
What are the specific surface molecules in the membrane of neighboring axons that bind tightly to each other, causing axons to grow in unison?
Cell-adhesion molecules (CAMs).
57
How do pioneer axons contribute to the formation of neural pathways?
Pioneer axons establish initial connections and guide neighboring axons as the nervous system expands.
58
What is the role of intermediate targets in the growth of pioneer axons?
Intermediate targets serve as waypoints, and the interaction between axons and intermediate targets helps guide axons in the correct direction.
59
How are pioneer axon trajectories organized during growth?
Pioneer axon trajectories are divided into short segments, each ending at an intermediate target, ensuring precise growth along specific paths.
60
What is the significance of connecting the dots in axon growth?
By connecting intermediate targets, pioneer axons eventually reach their final destination in a highly organized manner.
61
What determines the direction and amount of growth in axons?
Interactions of cell surface molecules on growth cones with guidance cues in the environment.
62
What are chemoattractants, and how do they work in axon growth?
Chemoattractants are diffusible molecules that attract growing axons toward their targets. They act over a distance, much like the aroma of coffee attracting a coffee lover.
63
What is the first identified chemoattractant in mammals?
Netrin, a protein secreted by neurons in the ventral midline of the spinal cord.
64
How does netrin work to attract axons?
Netrin binds to its receptors on axons, spurring growth toward the source of netrin, creating a gradient.
65
What is a chemorepellent, and how does it affect axon growth?
A chemorepellent is a diffusible molecule that repels axons. Slit is an example of a chemorepellent. Axons need to express the appropriate receptor (robo) to be repelled by chemorepellents.
66
How does the interaction between netrin and slit control axon growth?
Axons are initially attracted to the midline by netrin. Once they cross the midline, they encounter slit, which repels them. The presence of the appropriate receptor (robo) determines whether axons are attracted or repelled.
67
What is the role of permissive substrates in axon growth?
Permissive substrates are available for axon growth and help guide axons along their trajectory. In the provided example, midline cells serve as intermediate targets, alternating between attraction and repulsion for growing axons crossing the CNS.
68
What is the "choice point" for retinogeniculate axons?
The optic chiasm.
69
What happens to axons from the nasal and temporal retinas at the optic chiasm?
Axons from the nasal retina cross to the contralateral optic tract, while axons from the temporal retina remain in the ipsilateral optic tract.
70
What is the chemoaffinity hypothesis?
The idea that chemical markers on growing axons are matched with complementary chemical markers on their targets to establish precise connections
71
What is the significance of the retinotectal projection in frogs?
It receives retinotopically ordered input from the contralateral eye and helps organize movements in response to visual stimulation.
72
How did Sperry investigate how the retinotopic map was established in the tectum? What was the result of Sperry's experiment involving the regeneration of the optic nerve in frogs?
-He cut the optic nerve, rotated the eye 180° in the orbit, and allowed the upside-down nerve to regenerate.
-Despite the scrambled axons, they grew into the tectum to exactly the same sites they occupied originally, resulting in mirror-image vision.
73
What guides retinal axons to the correct part of the tectum?
Factors expressed in tectal cell membranes.
74
How do nasal retinal axons navigate the tectum?
They cross the anterior part of the tectum and innervate neurons in the posterior part
75
What about temporal retinal axons?
They grow into the anterior tectum and stop there.
76
What factors affect the growth of nasal and temporal retinal axons on tectal membranes?
Differential expression of factors on anterior and posterior tectal neurons.
77
What is one known repulsive signal for temporal retinal axons
Ephrins
78
Where are ephrins found in gradients across the tectum
The highest levels are on posterior tectal cells
79
How does ephrin interact with the growing axon?
It interacts with a receptor called "eph," inhibiting further axonal growth.
80
What does the expression of guidance cues and their axonal receptors impose on the wiring of the retina to its brain targets?
Topographic order.
81
What is often required for the final refinement of connections?
Neural activity.
82
What is the first step in synapse formation when a growth cone comes in contact with its target?
The induction of a cluster of postsynaptic receptors under the site of nerve-muscle contact.
83
What triggers the clustering of postsynaptic receptors at the neuromuscular junction?
An interaction between proteins secreted by the growth cone and the target membrane, with one of these proteins being agrin.
84
What is the role of agrin in synapse formation at the neuromuscular junction?
Agrin in the basal lamina binds to a receptor in the muscle cell membrane called muscle-specific kinase (MuSK) and stimulates the gathering of postsynaptic acetylcholine receptors (AChRs) at the synapse.
85
What regulates the size of the receptor "flock" at the neuromuscular junction?
Neuregulin, a molecule released by the axon, stimulates receptor gene expression in the muscle cell.
86
What triggers neurotransmitter release at the synapse?
Ca2+ entry into the growth cone, which is stimulated by basal lamina factors provided by the target cell.
87
What role does Ca2+ entry into the axon play in synapse formation?
It triggers neurotransmitter release and changes in the cytoskeleton of the axon, causing it to assume the appearance of a presynaptic terminal and adhere to its postsynaptic partner.
87
What are the key steps in synapse formation in the CNS?
Formation of dendritic protrusions, deposition of presynaptic active zones, recruitment of neurotransmitter receptors to the postsynaptic membrane, and the expression of specific adhesion molecules by both presynaptic and postsynaptic membranes.
88
What are the steps in formation of CNS synapses
(1) Dendritic filopodium contacts
axon
(2) Synaptic vesicles and active
zone proteins recruited to presynaptic membrane
(3) Receptors accumulate on
postsynaptic membrane
89
Why is a balance between the creation and elimination of cells and synapses important for proper brain function?
A balance between creating and eliminating cells and synapses is crucial for the development of proper brain function.
90
What significant refinement occurs during the development of the nervous system?
A large-scale reduction in the numbers of newly formed neurons and synapses is one of the significant refinements during nervous system development.
91
What is the process that eliminates entire populations of neurons during pathway formation?
Programmed cell death.
92
What leads to the decline in the number of presynaptic axons and neurons during synapse formation?
Competition for trophic factors, which are provided in limited quantities by target cells.
93
What does NGF stand for, and how does it influence neuronal survival?
NGF stands for Nerve Growth Factor. It is produced and released by the target tissue, taken up by sympathetic axons, and transported retrogradely, where it promotes neuronal survival.
94
What is the family of related trophic proteins that includes NGF?
The neurotrophins.
95
What are the receptors for neurotrophins, and how do they influence neuronal function?
The receptors are neurotrophin-activated protein kinases called trk receptors. They phosphorylate tyrosine residues on substrate proteins, stimulating a second messenger cascade that alters gene expression in the cell's nucleus.
96
How is cell death during development different from necrosis?
Cell death during development, called apoptosis, is a consequence of genetic instructions to self-destruct, while necrosis is accidental cell death resulting from injury.
97
Who discovered cell death genes, and what is their role?
Robert Horvitz discovered cell death genes. These genes cause neurons to die by apoptosis, a systematic disassembly process.
98
What is synaptic capacity? How does synaptic capacity change throughout development?
Synaptic capacity is the maximum number of synapses that a neuron's dendrites and soma can receive. Synaptic capacity peaks early in development and then declines as neurons mature.
99
How does the synaptic capacity of visual cortical neurons in infants compare to that of adults?
Visual cortical neurons in infants receive about 50% more synapses than those in adults.
100
What did Jean-Pierre Bourgeois and Pasko Rakic discover about synaptic capacity in the macaque monkey's striate cortex during adolescence?
Synaptic capacity in the striate cortex remains constant from infancy to puberty but declines sharply during adolescence
101
What is the average rate of synapse loss in the primary visual cortex during adolescence?
The loss of synapses in the primary visual cortex during adolescence occurs at an average rate of 5000 per second.
102
What process regulates synaptic elimination at the neuromuscular junction?
Electrical activity in the muscle regulates synaptic elimination at the neuromuscular junction.
103
What happens during the initial phase of synapse elimination at the neuromuscular junction?
The initial phase involves the loss of postsynaptic AChRs (acetylcholine receptors).
104
What causes the disappearance of AChRs at the neuromuscular junction?
Insufficient receptor activation in an otherwise active muscle causes the disappearance of AChRs
105
What is synaptic rearrangement?
Synaptic rearrangement refers to the change from one pattern of synapses to another within a neuron's synaptic capacity.
106
When does synaptic rearrangement typically occur? Synaptic rearrangement usually occurs as a consequence of neural activity and synaptic transmission in the developing brain.
-Synaptic rearrangement usually occurs as a consequence of neural activity and synaptic transmission in the developing brain.
-Sensory experience during childhood can profoundly influence synaptic rearrangement, particularly in the visual system.
107
What is the first step in the segregation of retinal inputs to the LGN?
The first axons to reach the LGN are usually those from the contralateral retina, and they spread out to occupy the entire nucleus.
108
What happens after the contralateral projection reaches the LGN?
Somewhat later, the ipsilateral projection arrives and intermingles with the axons of the contralateral eye.
109
How do the axons from the two eyes segregate in the LGN?
The axons from the two eyes segregate into the eye-specific domains that are characteristic of the adult nucleus.
110
What prevents the process of segregation in the LGN?
Silencing retinal activity with TTX (tetrodotoxin) prevents the process of segregation.
111
What is the source of retinal activity that orchestrates segregation in the LGN?
Ganglion cells are spontaneously active during fetal development, generating quasisynchronous "waves" of activity that spread across the retina.
112
What is the role of Hebbian modifications in synaptic plasticity during segregation?
Synapses that are active at the same time as their postsynaptic LGN target neurons are stabilized, and this process is known as Hebbian modification. It helps in the competition and elimination of stray retinal inputs.
113
How do inputs from the two eyes compete during segregation?
Inputs from the two eyes compete on a "winner-takes-all" basis until one input is retained and the other is eliminated based on correlation with postsynaptic responses.
114
What is ocular dominance column plasticity in visual cortex?
Ocular dominance columns are segregated regions in the visual cortex that process inputs from each eye. In monkeys and cats, their plasticity refers to the ability of these columns to change their width and organization based on visual experience
115
How are ocular dominance columns initially formed?
Ocular dominance columns are formed through molecular guidance cues and differences in retinal activity, mainly before birth.
116
What is monocular deprivation, and how does it affect ocular dominance columns?
Monocular deprivation is an experimental manipulation where one eyelid of a young monkey is sealed closed. It causes the "open-eye" columns to expand in width while the "closed-eye" columns shrink. This effect can be reversed by reopening the previously closed eye.
117
Is the plasticity of ocular dominance columns an activity-dependent or experience-dependent process?
The plasticity of ocular dominance columns is both activity-dependent and experience-dependent, as it relies on the quality of the sensory environment.
118
Does the plasticity of ocular dominance columns continue throughout life?
No, there is a critical period for this type of structural modification. In macaque monkeys, the critical period for anatomical plasticity in layer IV lasts until about 6 weeks of age. Afterward, the capacity for growth and retraction of LGN axons appears to be limited.
119
What is meant by "critical periods" during development?
Critical periods refer to specific times in development when environmental influences play a significant role in determining developmental outcomes. In the context of the visual cortex, critical periods are times when synaptic plasticity is particularly sensitive to visual experience.
120
What is the anatomical basis for binocular vision in species with ocular dominance columns?
The convergence of inputs from layer IV cells serving the right and left eyes onto cells in layer III.
121
When are binocular connections formed and modified under the influence of the visual environment?
During infancy and early childhood.
122
What does the establishment of binocular receptive fields depend on?
Correlated patterns of activity arising from the two eyes as a consequence of vision
123
What happens to the binocular connections in striate cortex when monocular deprivation occurs?
Monocular deprivation disrupts the binocular connections in striate cortex, and neurons with binocular receptive fields may respond only to stimulation of the nondeprived eye.
124
What is the term for the change in the binocular organization of the cortex caused by monocular deprivation?
Ocular dominance shift.
125
How rapidly can ocular dominance shifts occur in response to monocular deprivation?
Ocular dominance shifts can occur very rapidly, within hours of monocular deprivation, reflecting changes in synaptic structure and molecular composition
126
Does ocular dominance plasticity occur only in species with ocular dominance columns?
No, ocular dominance plasticity occurs in all mammals that have binocular vision, not just those with ocular dominance columns.
127
What is a hazard associated with activity-dependent fine-tuning of binocular connections?
These connections are highly susceptible to deprivation, which can disrupt binocular vision.
128
What is the consequence of disconnection in the striate cortex for an activity-deprived synapse?
In the striate cortex, disconnection of an activity-deprived synapse is not solely a consequence of disuse. Instead, it occurs due to a process of binocular competition where inputs from the two eyes actively compete for synaptic control of the postsynaptic neuron.
129
How does binocular competition in the visual cortex work?
In binocular competition, if the activity of both eyes is correlated and equal in strength, the inputs from both eyes are retained on the same cortical cell. However, if this balance is disrupted, such as by depriving one eye, the more active input will displace or weaken the deprived synapses.
130
What happens to the visual cortex in cases of strabismus?
Strabismus, a condition where the eyes are misaligned, can lead to competition between the inputs from the two eyes, causing patterns of activity to arrive out of sync in the cortex. This competition can result in the permanent loss of binocular receptive fields and a loss of stereoscopic vision.
131
What does the loss of binocular receptive fields following strabismus demonstrate?
The loss of binocular receptive fields following strabismus demonstrates that disconnection of inputs from one eye occurs due to competition between the eyes, rather than disuse. Even if both eyes are equally active, one input becomes dominant in each cortical cell, leading to a "winner takes all" scenario.
132
What are the consequences of an ocular dominance shift after monocular deprivation?
An ocular dominance shift after monocular deprivation leaves the animal visually impaired in the deprived eye.
133
What happens when there is a loss of binocularity associated with strabismus?
The loss of binocularity associated with strabismus completely eliminates stereoscopic depth perception.
134
Can the effects of ocular dominance shift and loss of binocularity be reversed?
Neither of these effects is irreversible if corrected early enough in the critical period.
135
What is the clinical recommendation regarding congenital cataracts or ocular misalignment in children?
Congenital cataracts or ocular misalignment must be corrected in early childhood, as soon as surgically feasible, to avoid permanent visual disability.
136
When does synaptic strengthening occur?
Synaptic strengthening occurs when the presynaptic axon is active, and the postsynaptic neuron is strongly activated by other inputs.
137
When does synaptic weakening occur?
Synaptic weakening occurs when the presynaptic axon is active, but the postsynaptic neuron is weakly activated by other inputs.
138
What does Hebb's hypothesis state?
Hebb's hypothesis states, "Neurons that fire together wire together."
139
What is the key factor for synaptic modification?
The key factor for synaptic modification is the correlation between synaptic activity and strong postsynaptic responses.
140
How are synapses "validated"?
Synapses are "validated" based on their ability to participate in the firing of their postsynaptic partner.
141
How can neurotransmitter receptors be classified based on their function?
Neurotransmitter receptors can be classified into two broad categories: G-protein-coupled, or metabotropic receptors, and transmitter-gated ion channels.
142
What is the distinguishing feature of NMDA receptors that sets them apart from AMPA receptors?
NMDA receptor conductance is voltage-gated, and their channels conduct Ca2+ ions. and AMPA receptors: glutamate-gated ion channels
143
What is the role of Mg2+ in NMDA receptor function?
At the resting membrane potential, Mg2+ blocks the NMDA receptor channel. Depolarization of the postsynaptic membrane displaces the Mg2+ block, allowing current to pass into the cell.
144
Why do "silent" synapses only become active when there is highly correlated activity?
"Silent" synapses contain NMDA receptors that only become active when there is sufficient depolarization, typically achieved through correlated activity.
145
What are NMDA receptors thought to detect?
Simultaneous presynaptic and postsynaptic activity.
146
What happens when NMDA receptors are strongly activated?
Long-term potentiation (LTP) occurs, strengthening synaptic transmission.
147
How does strong NMDA receptor activation lead to LTP?
It results in the insertion of new AMPA receptors into the synaptic membrane, making transmission stronger.
148
What additional change occurs following LTP induction?
Synapses can split in half, forming two different sites of synaptic contact.
149
In immature synapses, what receptors are present?
Clusters of NMDA receptors but few AMPA receptors.
150
How do synapses mature in cell culture?
They gain AMPA receptors over the course of development, but this change is blocked if NMDA receptors are antagonized
151
What is the mechanism behind this form of LTD?
Weak coincidences are signaled by lower levels of NMDA receptor activation and less Ca2+ influx, leading to synaptic plasticity called long-term depression (LTD), where active synapses are decreased in effectiveness.
152
What is one consequence of LTD induction?
One consequence of LTD induction is the loss of AMPA receptors from the synapse, which can lead to synapse elimination.
153
What does the loss of postsynaptic receptors stimulate at the neuromuscular junction?
The loss of postsynaptic receptors at the neuromuscular junction stimulates the physical retraction of the presynaptic axon.
154
How are AMPA receptors affected during monocular deprivation in the visual cortex? What is required for the loss of AMPA receptors during monocular deprivation?
-During monocular deprivation in the visual cortex, AMPA receptors are lost from the surface of visual cortical neurons.
-The loss of AMPA receptors during monocular deprivation requires residual activity in the deprived retina and activation of cortical NMDA receptors
155
How does eyelid closure during monocular deprivation affect retinal ganglion cell activity?
How does eyelid closure during monocular deprivation affect retinal ganglion cell activity?
156
What initiates the removal of AMPA receptors from the visually deprived synapse during monocular deprivation?
The modest entry of Ca2+ through NMDA receptors initiates a cascade of molecular events that leads to the removal of AMPA receptors from the visually deprived synapse.
157
What does the maintenance of connections formed during development depend on?
The maintenance of connections formed during development depends on their success in evoking an NMDA receptor-mediated response beyond a threshold level. Failure to achieve this threshold leads to disconnection.
158
What are the three hypotheses about why critical periods end?
-Plasticity diminishes when axon growth ceases.
Plasticity diminishes when synaptic transmission matures.
-Plasticity diminishes when cortical activation is constrained.
159
How does plasticity change in the adult brain compared to early development?
In the adult brain, plasticity is restricted to local changes in synaptic efficacy, whereas in early development, gross rearrangements of axonal arbors are possible.
160
What role do neurotransmitters like ACh and NE play in plasticity?
ACh and NE facilitate synaptic plasticity in the superficial cortical layers, possibly by enhancing polysynaptic intracortical transmission.
161
How does inhibition relate to the duration of the critical period?
Intrinsic inhibitory circuitry is late to mature in the striate cortex, and patterns of activity that may have gained access to modifiable synapses in early development might be tempered by inhibition in the adult. Manipulations that accelerate the maturation of inhibition can shorten the critical period, while those that slow its development can prolong it
