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202- Theme 1 > Chemicals in the brain > Flashcards

Chemicals in the brain Flashcards

1
Q

How are vesicles above the active zone anchored to the cytoskeleton in a synapse?

A

By the protein synapsin

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2
Q

What role does calcium play in synaptic vesicle release?

A

Activates calcium calmodulin activated kinase II which phosphorylates synapsin

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3
Q

What is the role of phosphorylated synapsin?

A

No longer binds to cytoskeleton so vesicles are free to dock to active zone

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4
Q

What does the SNARE complex do in synaptic vesicle transmission?

A

At active zone the SNARE complex docks vesicles to the plasma membrane.

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5
Q

What are the four stages of priming in exocytosis of neurotransmitter release?

A

a. vesicle docks
b. SNARE complexes form to pull membranes together
c. entering calcium binds synaptotagmin
d. Ca-synaptotagmin catalyses membrane fusion by binding SNAREs and plasma membrane

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6
Q

What occurs in congenital myasthenic syndrome?

A

Pre-synaptic terminal disease resulting in impaired vesicle recycling meaning less vesicles partake in NT release

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7
Q

What occurs in Latrotoxin?

A

Pre-synaptic terminal disease triggers vesicle fusion causing increase in available NT

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8
Q

What occurs in Botulin and Tetanus poisoning?

A

Pre-synaptic terminal affected. Affects SNARE proteins in vesicle fusion

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9
Q

What occurs to do with the presynaptic terminal in cognitive disorders?

A

Impaired transynaptic signalling

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10
Q

What occurs in presynaptic terminal disease LEMS?

A

Attacks presynaptic calcium channels. No increase in calcium so no SNARE complex forms

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11
Q

How does Botox act at the presynaptic terminal?

A

Acts directly at neuromuscular junction, affecting SNARE proteins so muscle loses all input and is permanently relaxed

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12
Q

How does Tetanus act at the presynaptic terminal?

A

Inhibits release of GABA and glycine at inhibitory neurons. Leads to disinhibition of cholinergic neurons causing permanent muscle contraction

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13
Q

What is the role of membrane transporters at the presynaptic terminal?

A

Enable neurotransmitters to enter vesicles as loaded against their concentration gradient

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14
Q

What is the role of vesicular transporters at presynaptic terminal?

A

Enable NT into vesicle. Powered by a proton gradient. ATPase proton pump loads vesicles with H+. Acidic vesicle compared to neutral cytoplasm facilitates 1 glutamate to be traded for 1 H+.

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15
Q

What is the role of plasma membrane transporters at presynaptic terminal?

A

Enable NT into presynaptic terminal. Powered by electrochemical gradient. High Na concentration outside and high K+ inside. Glutamate co-transported with 2 Na into plasma membrane of presynaptic terminal

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16
Q

What are the 4 categories of neurotransmitters?

A

Amino acids
Monoamines
Acetylcholine
Neuropeptides

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17
Q

What are the properties of small sized neurotransmitters? (amino acids, monoamines, acetylcholine)

A

synthesised locally in presynaptic terminal
stored in synaptic vesicles
released in response to local increase in calcium

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18
Q

what are the properties of neuropeptides? (small proteins)

A

synthesised in cell soma
transported to terminal
stored in larger secretory granules
released in response to global increase in calcium

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19
Q

what is the excitatory amino acid transmitter and where is it located?

A

Glutamate: in CNS

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20
Q

what are the inhibitory amino acid transmitters and where are they located?

A

GABA: brain
Glycine: spinal cord and brainstem

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21
Q

how is Glutamate synthesised?

A
  1. glucose via krebs

2. glutamine converted by glutaminase

22
Q

how is glutamate loaded and stored?

A

by vesicular glutamate transporters (VGLUTS)

23
Q

How is glutamate reuptaken

A

by excitatory amino acid transports located in pre-synaptic membrane and surrounding glia

24
Q

How is GABA synthesised?

A

from glutamate in reaction catalysed by glutamic acid decarboxylase

25
Q

How is GABA loaded and stored?

A

by vesicular GABA transporter (GAT)

26
Q

How is GABA reuptaken?

A

using transporters on glia and neurons including non-gabaergic neurons

27
Q

What occurs in cerebral ischaemia?

A

the electrochemical gradient is abolished, resulting in reversal of Na/K gradients. transporters release glutamate by reverse operation leading to excitotoxic cell death

28
Q

What is the result of GHB- the date rape drug?

A

It is a GABA metabolite that can be converted back to GABA resulting in increased GABA availability. causes unconsciousness and coma

29
Q

What are catecholamines and indolamines examples of?

A

Monoamines

30
Q

what are the two types of catecholamines?

A

Dopamine and norepinephrine

31
Q

How is dopamine formed?

A

Tyrosine (tyrosine hydroxylase) –> L-dopa (dopa decarboxylase) –> Dopamine

32
Q

How is epinephrine formed?

A

Dopamine (dopamine beta-hydroxylase) –> norepinephrine (phentolamine N-methyltransferase) –> epinephrine

33
Q

How are catecholamines stored and loaded into vesicles?

A

Loaded against concentration gradient via vesicular monoamine transporters (VMTs)

34
Q

How are catecholamines reuptaken?

A

reuptake into own axon terminal by transporters powered by electrochemical gradient: dopamine transporters (DATS) or norepinephrine transporters (NATS)
In the cytoplasm degraded by monoamine oxidases and inactivated by COMTs

35
Q

What is the mechanism of action of amphetamine?

A

reverses the transporter that reuptakes dopamine and norepinephrine. blocks its reuptake causing increased availability of neurotransmitter

36
Q

What is the mechanism of action of cocaine and methylphenidate?

A

blocks dopamine reuptake into terminals. increases amount in synaptic cleft so signal remains

37
Q

what is the mechanism of action of selegeline?

A

MAO inhibitor in dopaminergic nerve terminals. prevents degradation causing increased amount released on subsequent activations. treats early stages of PD

38
Q

What is the mechanism of action of entacapone

A

COMT inhibitor. dopamine not broken down. treatment for PD

39
Q

What type of monoamine is serotonin?

A

Indolamine

40
Q

How is serotonin synthesised?

A

Tryptophan (tryptophan hydroxylase) –> 5-HTP (5-HTP decarboxylase) –> 5-HT

41
Q

How is serotonin reuptaken?

A

By serotonin transporters (SERTs) on presynaptic membrane or destroyed by MAOs

42
Q

What is the mechanism of action of fluoxetine (prozac)?

A

Blocks serotonin reuptake. Is an SSRI

43
Q

What is the mechanism of action of fenfluramine?

A

stimulates serotonin release. inhibits reuptake

44
Q

What is the mechanism of MDMA?

A

NE + serotonin transporters run backwards, releasing NT into synapse

45
Q

How is acetylcholine synthesised?

A

Choline + acetyl CoA (choline acetyltransferase) –> acetylcholine

46
Q

What is the mechanism of action of neostigmine?

A

Acetylcholinesterase inhibitor: blocks breakdown of Ach to prolong its action. used to treat myasthenia gravis

47
Q

How is acetylcholine packaged into vesicles?

A

by vesicular Ach transporters (VAChT)

48
Q

How is ACh degraded in the synaptic cleft?

A

by acetylcholinesterase

49
Q

How are neuropeptides released?

A

by dense core vesicle fusion and exocytosis. in response to global increase in calcium. binds to and activates a receptor

50
Q

how are neuropeptides degraded?

A

signal terminated by diffusion from site of release and degradation by proteases

51
Q

How does NO work via retrograde signalling?

A

NO is made in postsynaptic neuron by NO synthase. Not stored so diffuses retrograde to presynaptic. activates guanyl cyclase–? cGMP. Switched off naturally by conversion to inactive form

202- Theme 1 (10 decks)

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