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Foundations 2 > PNP skeletal neuromuscular transmission > Flashcards

PNP skeletal neuromuscular transmission Flashcards

1
Q

curare

A

blocks twitch produced by nicotine and nerve stimulation

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2
Q

spark theory

A

theory in the early 1900s that thought neuron transmission was done through a direct electrical transfer of information

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3
Q

criteria needed to establish chimical rather than electrical transmission of nerve impulses

A

synthesis and storage

release

mimic effects of nerve stimulation with exogenous ACh

pharmacological parallels

termination

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4
Q

What experiment showed synthesis and storage of ACh?

A

acetylcholine was found in motor nerves

made through choline + acetyl CoA

choline acetyltransferase is the enzyme

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5
Q

What experiment showed release of ACh?

A

ACh could be collected after a nerve stimulation

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6
Q

What experiment showed mimicry?

A

ACh could be applied without the nerve firing and give rise to a muscle twitch

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7
Q

What are the pharmacological parallels of ACh?

A

drugs could emulate the stimulation of ACh, and curare could block the effects

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8
Q

What experiments showed termination?

A

acetylcholinesterases were shown to terminate the action of ACh

ACh -> choline + acetate

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9
Q

end plate

A

the direct synaptic area of the nerve onto the muscle

will have potentials that are not seen elsewhere in the muscle

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10
Q

end-plate potential

A

muscle response at the end-plate to a nerve impulse, needs to be sufficiently intense to generate an action potential

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11
Q

miniature end-plate potentials (MEPPs)

A

action potentials of the end-late that are generated without nerve impulse

due to spontaneous release of vesicles that provide quantums of a few thousand molecules of ACh

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12
Q

quantal hypothesis

A

the idea that EPPs are integral multiples of MEPPs due to the quantums of ACh that are released

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13
Q

How many quanta of ACh are released into the NMJ during a nerve impulse?

A

about 100 quanta

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14
Q

active zone

A

the area of the muscle where the nerve innervates

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15
Q

Describe the structures of the neuromuscular junction.

A
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16
Q

Describe the molecular process of an action potential.

A

vesicles are primed or “SNARED”

influx of calcium through a calcium channel due to action potential propagation

fusion of the vesicle with the membrane releases ACh

ACh binds to the post-synaptic ligand-gated sodium channel, which opens

an EPP is generated, if it is large enough it will activate voltage-gated sodium channels to produce a muscle twitch

ACh is degraded by acetylcholinesterases in the junction

17
Q

hemicholinium

A

blocks choline uptake, produces smaller MEPPs and smaller EPPs

18
Q

myasthenia gravis

A

smaller MEPPs than normal, caused by a reduction in the number of nicotinic ACh receptors

weakness and loss of control of muscles

can have difficulties eating and breathing

19
Q

TTX

A

blocks sodium channel responsible for upstroke both pre- and post- synaptically

20
Q

causes for the decreased influx of calcium ions via calcium channels in response to membrane depolarization

A

MG2+

aminoglycoside antibiotics

Lambert-Eaton myasthenic syndrome

21
Q

Mg2+ and calcium channels

A

along with other impermeant polyvalent cations such as Co2+, Mn2+, Cd2+, La3+ compete with Ca2+ at an external site that that allows Ca2+ entry

reduce neurally-evoked ACh release as well as other neurotransmitters

22
Q

aminoglycoside antibiotics

A

reduce evoked ACh release by reducing of Ca2+ entry through Ca2+ channels

23
Q

Lambert-Eaton Myasthenic Syndrom (LEMS)

A

disease associated with bronchogenic carcinoma

reflected as reduced number of ACh packets released by nerve impulses due to a reduced number of P/Q type Ca+ channels in the nerve ending

24
Q

black widow spider venom (BWSV)

A

active ingredient is alpha-latrotoxin

initially causes a huge asynchronouse barrage of vesicular exocytosis and MEPPs

several hours later, when all ACh release ends, nerve terminals are completely depleted of cholinergic synaptic vesicles

mechanism through increase in calcium channels in the nerve ending, creating an asynchronous rise in cytoplasmic calcium concentrations inr esponse to the venom

25
Q

botulinum toxin

A

enormously potent toxin that consists of 7 fractions

each fraction irreversibly cleaves a specific part of one of three SNAREs

prevents the priming of ACh release and thus preventing neurotransmitter release

26
Q

botulinum toxin type A (BOTOX)

A

most widespread clinical use - inhibits ACh release by reducing apparent affinity of calcium for the exocytosis process inside the nerve ending

target is a SNARE called SNAP-25, loosely associated with the nerve terminal membrane and linked to the calcium sensor so it can regulate the calcium sensitivity of secretion

27
Q

clinical uses of BOTOX

A

blepharospasm and other ocular disorders

hemifacial spasms

laryngeal problems such as stuttering or spasmodic dysphonia

diseases that produce peripheral spasticity in the legs, arms, and hands

spasms associated with repetitive activity such as musician’s cramp and writer’s cramp

autonomic focal hyperhydrosis and urinary incontinence

28
Q

What toxin produces effects similar to MG?

A

alpha-bungarotoxin

29
Q

characteristics of a post-junctional impairment

A

if EPP amplitudes, MEPP amplitudes, and the response to exogenous ACh are all decreased in parallel regardless of how ACh is applied

lack of responsiveness to ACh is post-junctional

30
Q

characteristics of a pre-junctional impairment

A

EPP amplitudes are decreased without a change in MEPP amplitudes (ratio of average EPP to average MEPP potentials is decreased)

decresae in evoked ACh release, very common phenomenon

31
Q

What are the three SNARE molecules that facilitate vescile fusion to the pre-synaptic membrane?

A

synaptobrevin

SNAP-25

syntaxin

32
Q

mechanistic function of Botx/A

A

cleaves SNAP-25 at amino acid 9 where it interacts with the calcium sensor

33
Q

Botx/B mechanism

A

cleaves synaptobrevin

34
Q

Botx/C mechanism

A

cleaves syntaxin

35
Q

synaptogamin

A

calcium sensor attached to the SNAREs

Foundations 2 (33 decks)

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