Somatic

Question 1

single neurone connecting the… to the …

Answer 1

CNS, skeletal muscle

Question 2

what receptors are found skeletal-muscle motor end plates?

Answer 2

nicotinic

Question 3

2 features about nicotinic receptors at the motor-end-plate

Answer 3

ligand gated ion channels, ACh binds at 2 places

Question 4

Na+ driven AP open up…

Answer 4

L-type Ca channels

Question 5

3 ways drugs interfere with ACh release at the NMJ

Answer 5

Block nAChR at NMJ, Decrease ACh at NMJ (inhibit synthesis/release) and Increase ACh or ACh effect at the NMJ

Question 6

how do NMJ blocking drugs work?

Answer 6

interfere with postsynaptic action of ACh

Question 7

2 different types of NMJ blocking drugs

Answer 7

NON-depolarising agents and DEPOLARISING agents

Question 8

how do non-depolarising agents work?

Answer 8

competitive antagonists at the ACh receptors

Question 9

examples of non-depolarising drugs

Answer 9

d-Tubocurarine, atracurium, α-bungarotoxin

Question 10

are non-depolarising drugs reversible?

Answer 10

yes, increase [ACh]

Question 11

unwanted effects of non-depolarising agents

Answer 11

hypotension

Question 12

how do depolarising agents work?

Answer 12

initially bind and activate the nicotinic receptors, and maintain a constant depolarisation at the end-plate, causing a loss of electrical excitability

Question 13

example of a depolarising agent

Answer 13

suxamethonium

Question 14

what is a side effect of the depolarising agents

Answer 14

initial fasciculation

Question 15

2 main stages of a depolarising agent

Answer 15

muscle held in depolarised state, desensitisation due to persistent stimulation

Question 16

neostigmine

Answer 16

competes with ACh on cholinesterase, causes parasympathetic stimulation and reverses non-depolarising block

Question 17

competitive inhibitor of choline uptake

Answer 17

hemicholinium (this will decrease the amount of ACh at the NMJ)

Question 18

inhibition of ACh transport

Answer 18

Vesamicol, blocks ACh transport into vesicles, so can’t be released

Question 19

False transmitters

Answer 19

triethylcholine - no depolarising actions

Question 20

block neuronal depolarisation

Answer 20

tetrodotoxin, blocks voltage gated Na+ channels, block AP

Question 21

Block neuronal Ca2+ influx

Answer 21

streptomycin/neomycin

Question 22

inhibition of vesicular fusion

Answer 22

botulinum toxin, β bungarotoxin, cleaves the SNARE proteins

Question 23

6 ways to decrease ACh at NMJ

Answer 23

inhibition of ACh synthesis, inhibition of ACh transport, false transmitters, block neuronal depolarisation, block neuronal Ca influx, inhibition of vesicular fusion

Question 24

2 methods for increasing ACh release and levels at the NMJ

Answer 24

δ-atrocotoxin - prolong neuronal Na+ channel opening, prolonging the AP AND Acetylcholinesterase inhbitors, so
ACh is not degraded (Edrophonium and Neostigmine)

Question 25

pralidoxime

Answer 25

can reactivate cholinesterases

Question 26

neostigmine

Answer 26

improve muscle contraction, used to treat myasthenia gravis