Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Medicine > Chemicals in the Brain > Flashcards

Chemicals in the Brain Flashcards

1
Q

Synaptic Vesicle release and recycling

  • Pool of vesicles above the active zone is anchored to the cytoskeleton by …
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates …. P-… can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • …* complex at active zone docks vesicles to the plasma membrane
A
  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Synaptic Vesicle release and recycling

  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated …+ channels open, …+ flows into cytoplasm
  • …+ activates … … activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
A
  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mechanisms of exocytosis during NT release

  • … and … on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - … complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to … and the plasma membrane
A
  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mechanisms of exocytosis during NT release

  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • … and SNAP-… on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering … ions binds to synaptotagmin
  • … bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
A
  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Synaptic vesicle release and recycling

  • After the exocytosis, vesicle membrane is rapidly recovered via …, new vesicles bud off and are refilled with transmitter
  • whole process takes … …
A
  • After the exocytosis, vesicle membrane is rapidly recovered via endocytosis, new vesicles bud off and are refilled with transmitter
  • whole process = 1 minute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cleavage of SNARE proteins by clostridial toxins

  • SNARE proteins important for NT to function
    • … toxin - affects transmission of Ach
    • … toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
A
  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of Ach
    • Tetanus toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cleavage of SNARE proteins by clostridial toxins

  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of …
    • … toxin - acts on interneurons as spinal cord (inhibitory) affect release of … and … - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
A
  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of Ach
    • Tetanus toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Botox and Tetanus - Prevent … release

A

Botox and Tetanus - Prevent transmitter release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Botox and Tetanus

  • Botox and Tetanus - Prevent … release
  • Botulinium and tetanus toxin - from bacteria Clostridium Botulinum and Tetani respectively
  • Botox acts directly at the … … - the muscles lose all input and so become permanently … (treatment of muscle …)
  • Tetanus toxin inhibits the release of .. and .. at inhibitory neurons, resulting in dis-inhibition of … neurons, which causes permanent muscle …
A
  • Botox and Tetanus - Prevent transmitter release
  • Botulinium and tetanus toxin - from bacteria Clostridium Botulinum and Tetani respectively
  • Botox acts directly at the NT junction - the muscles lose all input and so become permanently relaxed (treatment of muscle spasms)
  • Tetanus toxin inhibits the release of Glycine and GABA at inhibitory neurons, resulting in dis-inhibition of cholinergic neurons, which causes permanent muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diseases that affect the presynaptic terminal

  • Congenital … syndromes - impaired vesicle recycling
  • Another type of … - LEMS - attacks presynaptic Ca2+ channels
  • … disorders - impair transsynaptic signalling
  • …toxin - triggers vesicle fusion (black widow spider poison)
  • Botulinum and tetanus toxins - … proteins affected involved in vesicle fusion
A
  • Congenital myasthenic syndromes - impaired vesicle recycling
  • Another type of myasthenia - LEMS - attacks presynaptic Ca2+ channels
  • Cognitive disorders - impair transsynaptic signalling
  • Latrotoxin - triggers vesicle fusion (black widow spider poison)
  • Botulinum and tetanus toxins - SNARE proteins affected involved in vesicle fusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Membrane transporters - amino acids, amines and Ach

  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by … gradient:
    • … proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by … gradient
    • Na+ higher outside, K+ higher inside
    • … co-transported with 2 Na+
A
  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • Na+ higher outside, K+ higher inside
    • Glutamate co-transported with 2 Na+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Membrane transporters - amino acids, amines and Ach

  • Bringing back NT from … cleft to … neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • …+ higher outside, …+ higher inside
    • Glutamate co-transported with … Na+
A
  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • Na+ higher outside, K+ higher inside
    • Glutamate co-transported with 2 Na+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Glia

  • Majority of cells of brain >…%
  • Can release NT themselves and respond to them
  • Involve in many diseases - brain cancer, HIV, dementia
  • Very important - crucial for correct functioning of … but not enough known about them
A
  • Majority of cells of brain >80%
  • Can release NT themselves and respond to them
  • Involve in many diseases - brain cancer, HIV, dementia
  • Very important - crucial for correct functioning of synapses but not enough known about them
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Categories of Neurotransmitters:

  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in … terminal
    • Stored in … vesicles
    • Released in response to local increase in …+
  • Neuropeptides
    • Synthesized in the cell … and transported to the terminal
    • Stored in … granules
    • Released in response to global increase in …+
A
  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to local increase in Ca2+
  • Neuropeptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory granules
    • Released in response to global increase in Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Categories of Neurotransmitters:

  • Amino acids , … , …
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to … increase in Ca2+
  • …peptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory …
    • Released in response to … increase in Ca2+
A
  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to local increase in Ca2+
  • Neuropeptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory granules
    • Released in response to global increase in Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Neurotransmitters in the CNS

  • Fast e.g. … …
  • Slow e.g. …
A
  • Fast e.g. amino acids (GLUTAMATE/GABA)
  • Slow e.g. neuropeptides (Oxytocin,noradrenaline)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Amino acid NT - fast

  • …:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • …:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) - spinal cord and brain stem
A
  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) spinal cord and brain stem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

… neurotransmitters - slightly hyperpolarises the postsynaptic cell’s membrane

A

Inhibitory neurotransmitters - slightly hyperpolarises the postsynaptic cell’s membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Amino acid NT - fast

  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • … (…) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • … - brain
    • … (…) - spinal cord and brain stem
A
  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) spinal cord and brain stem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

… neurotransmitters - slightly depolarises the postsynaptic cell’s membrane

A

Excitatory neurotransmitters - slightly depolarises the postsynaptic cell’s membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GABA (brain) and glycline (spinal cord and brain stem) are both what type of neurotransmitter?

A

Inhibitory - slightly hyperpolarises the postsynaptic cell’s membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Glutamate (Glu) - CNS is what type of neurotransmitter?

A

Excitatory - slightly depolarises the postsynaptic cell’s membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diffuse modulatory systems e.g. the Serotonergic system

  • Function in: m…, sleep, p…, emotion, a..
  • Common principles : core
    • small set of neurons. most arise from … …
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
A
  • Function in: mood, sleep, pain, emotion, appetite
  • Common principles : core
    • small set of neurons. most arise from brain stem
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diffuse modulatory systems e.g. the Serotonergic system

  • Function in: mood, …, pain, …, appetite
  • Common principles : core
    • small set of neurons. most arise from … ….
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
A
  • Function in: mood, sleep, pain, emotion, appetite
  • Common principles : core
    • small set of neurons. most arise from brain stem
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
25
Q

Why have more NT’s?

A
  • 6 different layers of neuro-cortex - Different inputs and outputs
    • E.g top layers - feedback connections with other parts of cortex
    • 3 and 4 - mainly thalamus
    • 5 and 6 - cortical structure
  • Complexity in terms of wiring and inputs and outputs
26
Q

Glutamate - excitatory

  • Synthesized in presynaptic terminal from 2 sources
    • From glucose via the … cycle
    • From glutamine converted by glutaminase into glutamate
  • Loaded and … in vesicles by vesicular glutamate … (VGLUTs)
  • … by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia
  • Glial cells convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into glutamate
A
  • Synthesized in presynaptic terminal from 2 sources
    • From glucose via the Krebs cycle
    • From glutamine converted by glutaminase into glutamate
  • Loaded and stored in vesicles by vesicular glutamate transporters (VGLUTs)
  • Reuptake by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia
  • Glial cells convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into glutamate
27
Q

GABA (y-aminobutyric acid) - inhibitory

  • Synthesized from … (…) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by … using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than …
A
  • Synthesized from glutamate (Glu) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
    *
28
Q

GABA (y-aminobutyric acid) - inhibitory

  • Synthesized from glutamate (Glu) in a reaction catalyzed by … … … (GAD)
  • Loaded and stored into vesicles by a … … transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
A
  • Synthesized from glutamate (Glu) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
    *
29
Q

Regulation of amino acid transmitter release

  • Too much …/ too little … - hyper-excitability - epilepsy –> excitotoxicity
  • Too much … - sedation/coma
A
  • Too much Glu/ too little GABA - hyper-excitability - epilepsy –> excitotoxicity
  • Too much GABA - sedation/coma
30
Q

Cerebral ischemia - too much GLU

  • The metabolic events that retain the electrochemical gradient are abolished
  • Reversal of the Na+/K+ gradient
  • Transporters release … from cells by reverse operation
  • … -> cell death (large increase of Ca2+ -> enzymes -> digestion of overexcited cells - death)
A

Cerebral ischemia - too much GLU

  • The metabolic events that retain the electrochemical gradient are abolished
  • Reversal of the Na+/K+ gradient
  • Transporters release glutamate from cells by reverse operation
  • Excitotoxic -> cell death (large increase of Ca2+ -> enzymes -> digestion of overexcited cells - death)
31
Q

Cerebral ischemia - too much …

A

Cerebral ischemia - too much GLU

32
Q

GHB y-hydroxybutyrate (date rape drug) - too much …

A

GHB y-hydroxybutyrate (date rape drug) - too much GABA

33
Q

GHB y-hydroxybutyrate (date rape drug) - too much GABA

  • A GABA metabolite that can be converted back to GABA
  • Increases amount of available GABA
  • Too much = … and …
A
  • A GABA metabolite that can be converted back to GABA
  • Increases amount of available GABA
  • Too much = unconsciousness and coma
34
Q

The monoamines

  • … - dopamine, epinephrine, norepinephrine
  • … - serotonin
A
  • Catecholamines - dopamine, epinephrine, norepinephrine
  • Indolamines - serotonin
35
Q

The monoamines

  • Catecholamines - …, epinephrine, …
  • Indolamines - …
A
  • Catecholamines - dopamine, epinephrine, norepinephrine
  • Indolamines - serotonin
36
Q

Catecholamine synthesis I

  • Dopamine synthesis occurs in … steps
A
  • Dopamine synthesis occurs in 2 steps
37
Q

Catecholamine synthesis II

A
  • DBH located in synaptic vesicles only, and NE is the only transmitter synthesised within vesicles
38
Q

Administration of levodopa for treating what disease?

A

Parkinson’s disease (Levodopa - converted to dopamine in brain - can cross blood brain barrier)

39
Q

Levodopa - converted to dopamine in brain - can cross blood… …

A

Levodopa - converted to dopamine in brain - can cross blood brain barrier

40
Q

Catecholamine storage

  • Loaded into vesicles by Vesicular … … (VMATs) (proton gradient like Glu and GABA transporters)
  • Modulation of catecholamine synthesis by drugs:
    • L-DOPA - Levodopa - precursor of …, is used as a treatment for Parkinson’s. Dopa decarboxylase converts it into … increasing the pool of releasable transmitter
A
  • Loaded into vesicles by Vesicular monoamine transporters (VMATs) (proton gradient like Glu and GABA transporters)
  • Modulation of catecholamine synthesis by drugs:
    • L-DOPA - Levodopa - precursor of dopamine, is used as a treatment for Parkinson’s. Dopa decarboxylase converts it into dopamine increasing the pool of releasable transmitter
41
Q

Catecholamine release and reuptake

  • Released by Ca2+ dependant …
  • Binds and activates …
  • Signal terminated by … into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • … back into vesicles
    • Enzymatically degraded by … oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
A
  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by monoamine oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
42
Q

Catecholamine release and reuptake

  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by … OR
    • Inactivated by …
A
  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by monoamine oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
43
Q

Modulation of catecholamine release and reuptake by drugs:

  • … - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • … and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • s… - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • … - COMT inhibitor (treatment of PD)
A
  • Amphetamine - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - COMT inhibitor (treatment of PD)
44
Q

Modulation of catecholamine release and reuptake by drugs:

  • Amphetamine - reverses transporter so pumps out transmitter and blocks … (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA … into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - … inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - … inhibitor (treatment of PD)
A
  • Amphetamine - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - COMT inhibitor (treatment of PD)
45
Q

Serotonin (5-HT)

  • Synthesis:
A
46
Q

Serotonin storage, release and reuptake

  • … in vesicles
  • Signal terminated by … by Serotonin transporters (SERTs) on presynaptic membrane
  • Destroyed by … in cytoplasm
A
  • Stored in vesicles
  • Signal terminated by reuptake by Serotonin transporters (SERTs) on presynaptic membrane
  • Destroyed by MAOs in cytoplasm
47
Q

Drugs modulating serotonin release and reuptake

  • … (…) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • … stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • … - methylenedioxymethamphetamine - …: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
A
  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
48
Q

Drugs modulating serotonin release and reuptake

  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of … and …
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an … suppressant in the treatment of …
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in …)
A
  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
    *
49
Q

Acetylcholine - Ach

  • … … (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by … acetylcholine … (VAChT)
  • Rapidly … in synaptic cleft by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
A
  • Choline Acetyltransferase (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic clef by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
50
Q

Acetylcholine - Ach

  • Choline Acetyltransferase (ChAT, CAT) converts … + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic cleft by … (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
A
  • Choline Acetyltransferase (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic clef by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
51
Q

Drugs modulating acetylcholine degradation

  • AChE (acetylcholinesterase) …
    • Blocks the breakdown of Ach, prolonging its actions in the synaptic … e.g. neostigmine (treatment of myasthenia gravis, MG)
    • Positive - helps with … of disease
A
  • AChE (acetylcholinesterase) inhibitors
    • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. neostigmine (treatment of myasthenia gravis, MG)
    • Positive - helps with symptoms of disease
52
Q

AChE (acetylcholinesterase) inhibitors

  • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. … (treatment of myasthenia gravis, MG)
  • Positive - helps with symptoms of disease
A
  • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. neostigmine (treatment of myasthenia gravis, MG)
  • Positive - helps with symptoms of disease
53
Q

Neuropeptides

  • … transmission
  • Vary in their methods of … and release from small molecule transmitters
  • … polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
A
  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
54
Q

Neuropeptides

  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. e…, neuropeptide Y, substance P, endogenous opioids, v…
A
  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
55
Q

Neuropeptide release and degradation

  • Follow the … pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and … occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane … but not refilled
  • Bind to and activate …
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by .. in the extracellular environment
  • Release is … than small molecule release and signals may be maintained for …
A
  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and activate receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • Release is slower than small molecule release and signals may be maintained for longer
56
Q

Neuropeptide release and degradation

  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core … … and exocytosis occurs as a result of global elevations of …+ (sustained or repeated depolarization or release of …+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and … receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the … environment
  • Release is … than small molecule release and signals may be maintained for longer
A
  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and activate receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • Release is slower than small molecule release and signals may be maintained for longer
57
Q

Other transmitters/ retrograde signalling

  • Soluble gases - Nitric oxide and carbon monoxide
    • NO made in … neuron by Nitric oxide synthase (activated by the binding of Ca2+ and calmodulin)
    • The gas is not … but rapidly diffuses from it’s site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
    • Activates guanylyl cyclase which makes the … messenger cGMP
    • Within a few seconds of being produced NO is converted to biologically … compound (Switching off the signal)
    • Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers) how big is a neuron?
A
  • Soluble gases - Nitric oxide and carbon monoxide
    • NO made in postsynaptic neuron by Nitric oxide synthase (activated by the binding of Ca2+ and calmodulin)
    • The gas is not stored but rapidly diffuses from it’s site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
    • Activates guanylyl cyclase which makes the second messenger cGMP
    • Within a few seconds of being produced NO is converted to biologically inactive compound (Switching off the signal)
    • Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers) how big is a neuron?
58
Q

Other transmitters - retrograde signalling

  • Endocannabinoids
    • Small lipids which mostly cause reduced … release at certain inhibitory terminals
    • A cannabinoid is also the active component of …
A
  • Endocannabinoids
    • Small lipids which mostly cause reduced GABA release at certain inhibitory terminals
    • A cannabinoid is also the active component of marijuana (Cannabis sativa)

Year 2 Medicine (162 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions