Neuromuscular Junction Flashcards

1
Q

what are the five steps of synaptic transmission
5 possible targets of drugs and toxins

A

synthesis of neurotransmitters
storage of neurotransmitters in vesicles
exocytosis of transmitters
transmitters bind to post-synaptic receptors
transmitters dissociate

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2
Q

why are neurotransmitters stored in vesicles in the pre-synaptic neuron

A

prevent them from metabolism
package them together

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3
Q

what causes exocytosis of transmitters from pre-synaptic neurons

A

opening of voltage-gated calcium channel

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4
Q

what do transmitters do when they bind post-synaptic receptors?

A

cause conformational changes
change the activity of the receptor

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5
Q

what facilitates transmitter dissociation
what happens to them afterwards

A

enzymes
broken down into components, some recycled

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6
Q

what is an agonist

A

substances which bind specific receptors and elicit a biological response

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7
Q

agonists:
affinity?
efficacy?
Reversible?

A

posses affinity and efficacy
always reversible

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8
Q

what is an antagonist

A

substances which bind specific receptors and do not activate them

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9
Q

antagonists:
affinity?
efficacy?
Reversible?

A

posses affinity but lack efficacy
not always reversible

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10
Q

which has higher binding affinity, antagonists or agonists?
how can the other still bind first

A

antagonists tend to have a higher affinity
agonists can bind first if at a higher concentration

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11
Q

what are the two moieties of acetylcholine

A

acetyl moiety
choline moiety

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12
Q

which subunit of nicotinic receptors does ACh bind
transmitter gated Na+ ion channels

A

alpha

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13
Q

how can a Na+ ion channel be isolated from a post-synaptic neuron

A

patch-clamp

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14
Q

how can mepps and epps be measured

A

microelectrodes

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15
Q

explain mepps

A

miniature end plate potentials
spontaneous depolarisations
depolarisation caused by a single vesicle
not sufficient to cause an AP

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16
Q

explain epps

A

end plate potentials
large depolarisation of the endplate of muscle cell
can initiate APs
summation of mepps in response to nerve impulse
muscle contraction

17
Q

how and why is the size of epps reduced for study

A

using a high Mg2+, low Ca+ buffer (Mg blocks Ca2+ channels, calcium triggers exocytosis)
prevent the glass microelectrode from breaking

18
Q

what does quantal mean in relation to transmitter release?

A

the amplitude of the epp is a multiple of the amplitude of the mepp
smallest epp = mepp

19
Q

what is quantal content
how is it calculated

A

number of vesicles per stimulation
QC=mean EPP amplitude / mean MEPP amplitude (mV)

20
Q

what enzyme synthesises ACh and from what

A

Choline acetyltransferase (CAT)
from choline and acetyl-CoA

21
Q

explain the reuptake of choline

A

Na+ dependant
blocked by hemichlonium 3

22
Q

effect on mepp, epp and QC if transmitter synthesis is blocked

A

less Ach per vesicle
-mepp and epps decreased equally
-no change in QC

23
Q

explain storage of ACh

A

transported into vesicles
blocked by inhibition of transporter

24
Q

effect on mepp, epp and QC if ACh storage is blocked

A

less Ach per vesicle
-mepp and epps decreased equally
-no change in QC

25
explain the process of vesicle exocytosis
AP causes the opening of Na+ channels depolarisation causes the opening of Ca2+ channels Calcium enters the cell and causes vesicles to move towards the synapse and fuse with the membrane depolarisation also causes the opening of K+ channels K+ exits the cell leading to repolarisation
26
target and effect of tetrodotoxin
blocks Na+ channels no action potential - no release - no epp no effect on mepps
27
target and effect of conotoxins
blocks Ca2+ channels less influx - less release - decreased epp no effect on mepp - lower QC
28
target and effect of dendrotoxin
blocks K+ channels prolonged APs - greater release - increased epp no effect on mepp - QC increased
29
target and effect of botulinum toxin
blocks vesicular fusion with the membrane decreased release - decreased epp no effect on mepp - QC decreased
30
target and effect of tubocurarine how can it be reversed
blocks nicotinic ACh receptors (antagonist) prevents sufficient Na+ influx for an AP paralyses skeletal muscle - decrease mepp and epp treated with neostigmine
31
target and effect of alpha-bungarotoxin how can it be reversed
blocks nicotinic ACh receptors (antagonist) prevents sufficient Na+ influx for an AP paralyses skeletal muscle - decrease mepp and epp irreversible
32
target and effect of succinylcholine
agonist of nicotinic ACh receptors leads to paralysis by rapidly and repeatedly binding and leading to desensitization
33
what is the effect of anticholinesterases
increase the effects of ACh prolonged APs
34
what are anticholinesterases used for
reverse muscle relaxants treat myasthenia gravis and Alzheimer's
35
target and effect of organophosphates
bind acetylcholine esterase and prevent its action recovery requires the synthesis of new enzymes (weeks)
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