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MSS - MSK Exam 3 > The NMJ From a Pharmacological Perspective > Flashcards

The NMJ From a Pharmacological Perspective Flashcards

1
Q

what to know?

A

put out notes packet** read it

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2
Q

junctional transmission

A

cholinergic > bc ACh is neurotransmitter

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3
Q

4 important steps in junctional transmission

A

synthesis of ACh
storage
release
degradation

*every neurotransmitter undergoes this process

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4
Q

4 steps in NMJ neurotransmission?

A

axonal conduction
junctional transmission
ACh signaling
muscle contraction

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5
Q

when does junctional transmission occur?

A

when axonal signal reaches terminal

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6
Q

what is activated by ACh?

A

nAChR

nicotinic acetylcholine receptors

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7
Q

choline transporter

A

membrane channel transports choline into cell
choline is precursor to ACh

cotransport of Na+ and choline into cell

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8
Q

choline acetyltransferase

A

ChAT

enzyme that combines acetyl CoA and choline to form ACh

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9
Q

hemicholinium

A

blocks the choline transporter

**don’t need to know - bc its used in labs, not clinically

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10
Q

patients with alzheimers?

A

reduced cerebral production of ChAT

-therefore have less formation of ACh

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11
Q

therapy for alzheimers?

A

to increase ACh levels**

-to make up for loss of low levels

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12
Q

ACh vesicular transporter

A

shuttles ACh into storage vesicle
**requires ATP

1-5K ACh per vesicle

motor nerve terminal may have over 300K vesicles

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13
Q

voltage-gated Ca2+ channels

A

open with depolarization and allow Ca2+ entry into cell

promote vesicle membrane fusion

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14
Q

VAMP and SNAPs

A

vesicular and membrane proteins that initiate vesicle-plasma membrane fusion and release of ACh

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15
Q

how many vesicles fuse per AP?

A

approximately 125 vesicles

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16
Q

VAMP

A

vesicle associated membrane protein

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17
Q

SNAP

A

synaptosome associated proteins

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18
Q

what are components of SNARE complex

A

VAMP-SNAP

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19
Q

what does botulinum do?

A

cleaves the SNARE complex so you can’t have vesicle fusion and ACh release

paralyzes muscles**

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20
Q

how long for fusion?

A

matter of milliseconds

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21
Q

acetylcholinesterase

A

AChE
enzyme that cleaves ACh
-into acetate and choline

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22
Q

choline transporter

A

recycles choline back into motor neuron

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23
Q

endocytosis?

A

occurs at nerve terminal to replenish the number of available vesicles

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24
Q

two sets of receptors for ACh?

A

nicotinic and muscarinic

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25
Q

nAChR

A

nicotinic ACh receptor
-also activate by nicotine

ligand gated ion channels (FAST)
sodium to flow into cell
-found pre and post junctionally

causes muscle AP and muscle contraction

26
Q

mAChR

A

muscarinic ACh receptor

  • also activated by muscarine
  • found pre and post junctionally

G-protein coupled receptors (SLOW)
NOT located at skeletal NMJ**

27
Q

nAChR distribution

A

skeletal muscle
cause contraction
respond to ACh and nicotine

28
Q

mAChR distribution

A

smooth muscle
cause contraction
respond to ACh and muscarine

in cardiac muscle (SA and AV node)

  • also on atrium and ventricle
  • decreased HR, conduction velocity, contraction
29
Q

subtypes of mAChR

A

5 in mammals M1-M5

activation is metabotropic

30
Q

metabotropic

A

causes second messenger pathway

31
Q

ionotropic

A

nAChR type

  • ligand gated ion channel
  • allows ions to pass through the channel pore
  • in this case, sodium ions**
32
Q

structure of nAChR

A

four-five distinct subunits

ACh binding occurs between alpha and adjacent subunit

requires binding of two ACh

subunits different depending on location of receptor
**allows for specific targeting in body of drugs

33
Q

subtypes of nAChR

A

skeletal muscle Nm

peripheral neuronal Nn
central neuronal

34
Q

skeletal muscle Nm subtype

A

at NMJ
excitatory > contraction
increased cation permeability

antagonists:
atracurium
vecuronium
d-tubocurarine
pancuronium
35
Q

succinyl choline

A

causes very fast paralysis

even though its an agonist of Nm AChR, its acts as an antagonists

-tires out the receptors

36
Q

what allows for specificity?

A

different subunit make up

37
Q

what passes through nAChR channel?

A

sodium, potassium, calcium ???

sodium is main mover, which depolarizes and initiates an AP

38
Q

prejunctional activation?

A

nAChR help to mobilize more vesicles
-physiological role confusing

on the presynaptic membrane***

mAChR activation results in ACh-mediated inhibition of further ACh release

39
Q

tetrodotoxin

A

inhibits voltage gated Na+ channels and prevents axonal conduction in motor neuron

no AP down neuron - paralysis

40
Q

local anesthetics

A

inhibits voltage-gated Na+ channels prevent axonal conduction

41
Q

diaphragm

A

skeletal muscle

42
Q

batrachotoxin

A

causes an increase in permeability of Na+ channels and induces a persistent depolarization
-one of the most potent toxins

43
Q

botulinum toxin

A

cleaves components of SNARE
-VAMP and SNAP proteins

stop vesicular fusion

44
Q

curare alkaloids

A

non-depolarizing competitive nAChR antagonist

45
Q

succinylcholine

A

depolarizing nAChR agonist

only acts on the Nm (skeletal muscle) nAChR

-but acts as antagonist (tires out receptor)

46
Q

neuromuscular blocking drugs

A

used for causing muscle paralysis during anesthesia induction

curare and succinylcholine

47
Q

cholinesterase inhibitor

A

increase concentration of ACh at NMJ

organophosphates
-activate smooth and skeletal muscles

used in lower concentration therapeutically

48
Q

therapeutic use of low concentration cholinesterase inhibitor?

A

dementia, alzheimers, parkinsons, myasthenia gravis, reversal of neuromuscular blockade during anesthesia

49
Q

myasthenia gravis

A

decreased in nAChR on surface of cell

-cholinesterase inhibitor will increase ACh to activate the decreased nAChR

50
Q

tetrodotoxin

A

also affects sodium channels on muscle cells (inhibits APs)

51
Q

dantrolene

A

inhibits ryanodine receptor in SR

  • blocks release of Ca2+
  • no contraction
52
Q

clinical use of dantrolene?

A

malignant hyperthermia, spasticity with upper motor neurons

53
Q

uptake of choline

A

rate limiting step

54
Q

endoytosis of vesicles

A

facilitated by clathrin

55
Q

tertodotixin

A

puffer fish toxin

blocks axonal conduction
-blocks Na+ channels (not used clinically)

56
Q

local anesthetics

A

block neuronal conduction
-inhibits Na+ channels

used for pain control during variety of clinical procedures

57
Q

botulinum

A

cleaves components of core SNARE complex
-prevents ACh release

treatments:
-strabismus
-blepharosmam with dystonia
-cervical dystonia
-wrinkles of face
-
58
Q

curare alkaloids

A

non-depolarizing competitive nAChR antagonist

during anesthesia to relax skeletal muscle

59
Q

succinylcholine

A

neuromuscular blocking drug

binds to nAChR - acts as an agonust
-continued depolarization leads to receptor blockade and paralysis

60
Q

dantroleine

A

inhibits ryanodine receptors in SR
-blocks Ca2+ release

malignant hyperthermia
spasticity with upper motor neurons
-spinal cord unjury, stroke, cerebral palsy, MS

MSS - MSK Exam 3 (16 decks)

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