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bioregulatory systems 🦠 > neurotransmitters and pharmacology > Flashcards

neurotransmitters and pharmacology Flashcards

1
Q

what does information transfer across a synapse require

A

a neurotransmitter and their interaction with postsynaptic receptors

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2
Q

summarise synaptic transmission in 4 steps

A

1) NT release from 1st cell
2) synaptic activation of 2nd cell
3) signal integration and signal conduction by 2nd cell
4) signal transmitted to effectors or subsequent neurones

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3
Q

4 features of synaptic transmission

A

rapid timescale
diversity of CNS function
plasticity
learning and memory

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4
Q

what is the structure of a neuron and how does it relate to synaptic transmission

A

dendrite (spines where info is received)
soma (body where info is integrated)
axon and synaptic terminals (where info is transferred rapidly by AP)

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5
Q

what is the soma

A

cell body

every neurone has one

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6
Q

what is the end of the axon called

A

synaptic terminal

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7
Q

what do dendrites have that increase SA for info receiving

A

proteins called spines

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8
Q

what does the cell body do

A

integrate info

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9
Q

what is AP

A

electrical transmission

chemical transmission occurs at the synaptic cleft

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10
Q

how big is the synaptic gap/cleft

A

20-100nm

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11
Q

STEPS for NT (3)

A

1) biosynthesis, packing and release of NT
2) NT released by exocytosis and receptor action on post synaptic neuron
3) inactivation of NT after activation on receptor

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12
Q

what are 3 types of NTs within the central nervous system

A

amino acids
amines
neuropeptides

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13
Q

examples of amino acid neutrotransmitters

A

gluatamate
GABA
glycine

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14
Q

examples of amine neurotransmitters

A

noradrenaline

dopamine

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15
Q

examples of neuropeptide neurotransmitters

A

opioid peptides

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16
Q

STEPS for activation of a CNS synpase

A

1) arrival of AP
2) spreads across nerve terminal
3) activates depolarisation of entire nerve terminal (rapid Na+ influx and K+ efflux) which activates VGCCs > Ca2+ enters and goes to nerve terminal > activates exocytosis of vesicle with NT
4) released into the cleft
5) rapidly diffuses across gap down gradient
6) binds to receptors on postsynaptic membrane > excitatory synapse as receptors allow influx of Na+ into postsynaptic cell > depolarisation of postsynaptic cell and generation of another AP > passes down axon
7) NT generated response > inactivate rapidly (reuptake of NT)
8) activation of Na+/K+ pump > extrudes Na+ that came in and replaces it with K+ (functions independently of reuptake system)
9) or enzyme degradation in cleft eg acetylcholinesterase to break down acetylcholine

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17
Q

where is acetylcholinesterase found

A

bound to basolateral membrane in synaptic cleft

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18
Q

what does neurotransmitter release need

A

an increase in intracellular Ca2+ as it is calcium dependent

requires rapid transduction

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19
Q

what is electromechanical transduction

A

links opening of calcium channel > influx > NT release into cleft

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20
Q

SUMMARY of NT release

A 
membrane depolarisation
Ca2+ channels open
Ca2+ influx
vesicles are primed
vesicle fusion
vesicle exocytosis
NT release
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21
Q

where are synaptic vesicles filled with NT docked

A

into synaptic zone

22
Q

what enables vesicle fusion and exocytosis on vesicles and presynaptic membranes

A

special proteins

eg SNARE proteins (vesicular proteins) mediating process of exocytotic release of NT

23
Q

what are targets for neurotoxins

A

vesicular proteins

24
Q

example of neurotoxin = alpha latrotoxin

A

black widow spider
stimulates NT release to depletion
binds to cholinergic terminal and causes release of ACh until depletion leading to muscular paralysis

25
Q

example of neurotoxin = Zn2+ dependent endopeptidases

A

inhibit NT release eg tetanus toxin (inhibits GABA release and glycine release leading to spasms and paralysis)

26
Q

example of neurotoxin = botulinum toxin

A

C botulinum - generating botulinum toxin > can cause arrest
causes flaccid paralysis
made of 2 chains
1st chain binds to cholinergic nerve terminal
2nd chain penetrates the cholinergic nerve terminal and interacts with vesicular proteins
cleaves peptide bonds of vesicular proteins
can no longer dock/fusion/release of NT - inactivated

27
Q

what are the 2 main groups of receptors

A

ion channel linked receptors (FAST)

G protein coupled receptors (SLOW)

28
Q

what are ion channel linked receptors and examples

A

receptors that produce fast response
mediate all fast excitatory and inhibitory transmission
glutamate binds to receptor > stimulation > opening allowing influx of Na+ into cell > AP
GABA (CNS)
neuromuscular junction - ACh at nicotinic receptors

29
Q

what are G protein coupled receptors

A

slow response
effectors may be :
- enzymes (adenyl cyclase, phospholipase C, cGMP-PDE)
- channels (eg Ca2+/K+)
examples
CNS and PNS : ACh at muscarinic receptors, dopamine (DA), noradrenaline (NA), serotonin (SHT) and neuropeptides (eg enkephalin)

30
Q

how do G protein coupled receptors work (STEPS)

A

1) stimulated by agonist
2) bind to G protein in membrane
3) G protein couples to receptor
4) second messenger in cell

31
Q

features of ion channel linked receptors

A

rapid activation
rapid info flow
multiple subunit combinations > distinct functional properties

32
Q

what is the ion channel linked receptor for acetylcholine

A

nicotininc cholinergic receptors (nAChR)

33
Q

what is the ion channel linked receptor for glutamate

A

GluR

34
Q

what is the ion channel linked receptor for GABA

A

GABAR

35
Q

what is the ion channel linked receptor for glycine

A

GlyR

36
Q

how many subunits are there

A

around 5

37
Q

GABA A receptors are..

A

inhibitory

38
Q

glutamate receptors lead to..

A

depolarisation

39
Q

STEPS for excitatory NT receptor

A

eg glutamate receptor
release of glutamate activating receptor on postsynaptic membrane
rapid influx of Na+ through channel (sometimes through receptor itself) down EC gradient
shoots into postsynaptic nerve
generates EXCITATORY POSTSYNAPTIC POTENTIAL (EPSP)

40
Q

STEPS for inhibitory NT receptor

A

eg GABA
binds to GABAR
opens Cl- channel
Cl- enters
fall in membrane potential (hyperpolarisation)
leads to INHIBITORY POSTSYNAPTIC POTENTIAL

41
Q

what exists between GABA and glutamate

A

a balance in the brain

42
Q

what are the 2 types of glutamate receptors

A

AMPA receptors

NMDA receptors

43
Q

describe AMPA receptors

A

majority of FAST excitatory synapses

rapid onset, offset and desensitisation

44
Q

describe NMDA receptors

A

slow component of excitatory transmission

serve as coincidence detectors which underlie learning mechanisms

45
Q

STEPS for excitatory glutamate synapse

A

1) glutamate synthesised from glucose via TCA cycle and transamination
2) glutamate reversibly binds postsynaptic receptors (linked to ion channels)
3) rapid uptake of glutamate by excitatory amino acid transporters (EAATs) excitatory AA transporters
4) glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells

46
Q

what receptors are found in the hippocampus

A

NMDA receptors

47
Q

what are seizures

A

abnormal cell firing > seizures associated with excess glutamate in synapse
glutamate returns to normal levels > increase in glutamine levels (metabolised glutamate)

48
Q

what is epilepsy

A

characterised by recurrent seizures due to abnormal neuronal excitability
disease can be disabling
25-30% refractory to treatment
new gen of drugs targeting GABA synapse

49
Q

STEPS for inhibitory GABA synapse

A

1) GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD)
2) GABA reversibly binds postsynaptic receptors (linked to ion channels)
3) rapid uptake of GABA by GABA transporters (GATs)
GABA enzymatically modified by GABA transaminase (GABA-T) to succinic semialdehyde (glial cells and GABA nerve terminals)

50
Q

what does GABA do to action potentials

A

reduce AP frequency

harder to induce AP

51
Q

structure of GABA receptor

A

pentameric organisation of GABA receptor > pharmacologically important binding domains

52
Q

what are some drugs facilitating GABA transmission

A 
antiepileptic
anxiolytic - reduce anxiety
sedative
muscle relaxant
enhance GABA inhibitory action

bioregulatory systems 🦠 (54 decks)

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