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MSK-1 > Pharmacology of NMJ > Flashcards

Pharmacology of NMJ Flashcards

1
Q

What is the ACh vesicular transporter?

A

ATP-dependent transporter that moves ACh into storage vesicles after synthesis

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2
Q

Where are mAChR?

A

Smooth muscle

cardiac muscle

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3
Q

What do curare alkaloids (tubocurarine) cause symptom-wise?

A

flaccid paralysis of skeletal muscles

used during anesthesia

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4
Q

How are the affects of tubocurarine reversed?

A

by increasing ACh in NMJ = AChE inhibitor

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5
Q

Would a AChE inhibitor used to treat myasthenia gravis be charged or uncharged?

A

charged - want to only affect skeletal muscle NMJs

if you use uncharged molecules, could affect CNS - not what you want here

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6
Q

What are the 2 agents that affect depolarization?

A 
curare alkaloids (d-tubocurarine) = antagonist
succinylcholine = agonist
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7
Q

How do curare alkaloids work?

What is the prototype?

A

antagonists for nicotinic receptor: compete w/ ACh –> decrease size of the EPP = no synaptic transmission
prototype = d-tubocurarine

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8
Q

How is ACh removed from IMJ?

A

Acetylcholinesterase (AChE) cleaves ACh into choline and acetate
Choline recycled back into motorneuron

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9
Q

What are symptoms of tetanus?

A

spastic paralysis, lockjaw
autonomic overactivity
rigid muscles

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10
Q

What does a muscarinic receptor cause in smooth muscle?

A

contraction

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11
Q

How does succinylcholine work?

A

agonist of nicotinic receptor:

binds to receptor and causes continued depolarization –> eventual paralysis

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12
Q

Why are nAChRs selective for the ions they allow through?

A

negatively charged AAs line pore –> affinity for positively charged ions = mainly Na+

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13
Q

What are the 2 agents that affect veisicular ACh release/

A

Botulinum toxin

tetanus toxin

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14
Q

What receptor is a ligand-gated ion channel?

A

nicotinic AChRs

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15
Q

Where is tetanus found and how does it work?

A

found in soil
blocks fusion of synaptic vesicles by targeting synaptobrevin (a SNARE protein)
after binding to presynaptic memrane, it is internalized and transported retroaxonally to spinal cord

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16
Q

What is myasthenia Gravis?

What are hallmark symptoms?

A

Autoimmune disorder where Ab attack nicotinic receptors
ptosis (droopy eyelids), fatigue that worsens throughout day and w/ activity
neural conduction, sensory, and autonomic responses are normal

17
Q

Once Ca enters the pre-synaptic neuron upon depolarization, what proteins help vesicle-PM fusion?
What type of proteins are they?

A

VAMP and SNAPs

Plasma membrane proteins

18
Q

How does dantrolene work and what are its clinical uses?

A

inhibits ryanodine receptors in SR of muscle cells –> no calcium release –> no muscle contraction

treats malignant hyperthermia, spasticity assoc w/ upper motor neuron disorders

19
Q

Where are nicotinic AChR?

What do they cause in the post-synaptic tissue?

A

skeletal muscle, peripheral neuronal, central neuronal

contraction

20
Q

When is succinylcholine used and what are its hallmark effects?

A

used as an induction agent for anesthesia
fast and short acting
causes muscle fasciculations and then paralysis

21
Q

What are agonists of skeletal muscle nicotinic receptors?

A

ACh
nicotine
Succinylcholine

22
Q

What is the mechanism of ACh synthesis?

A

Choline enters cell via choline transporter –> Choline acetyltransferase (ChAT) combines choline w/ Acetyl CoA –> ACh

23
Q

How do you treat Myasthenia Gravis?

A

use AChE inhibitor –> more ACh at NMJ can restore some normal function

24
Q

What is the antagonist of Peripheral neronal and central neronal nicotinic receptors?

A

mecamylamine

25
Q

What is tetrodoxin and how does it work?

A

puffer fish poison

Inhibits voltage-gated Na+ channels on neuron –> no axonal conduction

26
Q

What are antagonists of skeletal muscle nicotinic receptors?

A

d-tubocurarine
atracurium
vecuronium
pancuronium

27
Q

What does a muscarinic receptor cause in cardiac muscle?

A

decreased:

HR, conduction velocity, contraction

28
Q

How does the botulinum toxin work?

A

cleaves components of SNARE complex –> ACh cant be exocytosed –> no muscle contraction

29
Q

About how many vesicles rupture per AP?

A

125

30
Q

What disease causes reduced cerebral production of ChAT? What would this in turn cause?

A

Alzheimers

less production of Acetylcholine

31
Q

How do local anaesthetics work?

A

inhibit voltage-gated Na channels on neuron –> no AP

32
Q

What are symptoms of botulism?

A

acute onset of bilateral cranial neuropathis w/ symmetric descending weakness
no sensory deficits except blurred vision
nausea, vomiting, abdominal pain, diarrhea, dry mouth

33
Q

When is an AChE inhibitor used?

A

to increase concentration of ACh at NMJ
treats: dementia assoc w/ alzheimer or parkinson’s; myasthenia gravis, nerve gas and pesticide exposure, reversal of anesthesia

MSK-1 (28 decks)

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