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

The NMJ From a Pharmacological Perspective Flashcards

(60 cards)

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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
nAChR
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
mAChR
muscarinic ACh receptor - also activated by muscarine - found pre and post junctionally G-protein coupled receptors (SLOW) NOT located at skeletal NMJ**
27
nAChR distribution
skeletal muscle cause contraction respond to ACh and nicotine
28
mAChR distribution
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
subtypes of mAChR
5 in mammals M1-M5 activation is metabotropic
30
metabotropic
causes second messenger pathway
31
ionotropic
nAChR type - ligand gated ion channel - allows ions to pass through the channel pore - in this case, sodium ions**
32
structure of nAChR
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
subtypes of nAChR
skeletal muscle Nm peripheral neuronal Nn central neuronal
34
skeletal muscle Nm subtype
at NMJ excitatory > contraction increased cation permeability ``` antagonists: atracurium vecuronium d-tubocurarine pancuronium ```
35
succinyl choline
causes very fast paralysis even though its an agonist of Nm AChR, its acts as an antagonists -tires out the receptors
36
what allows for specificity?
different subunit make up
37
what passes through nAChR channel?
sodium, potassium, calcium ??? sodium is main mover, which depolarizes and initiates an AP
38
prejunctional activation?
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
tetrodotoxin
inhibits voltage gated Na+ channels and prevents axonal conduction in motor neuron no AP down neuron - paralysis
40
local anesthetics
inhibits voltage-gated Na+ channels prevent axonal conduction
41
diaphragm
skeletal muscle
42
batrachotoxin
causes an increase in permeability of Na+ channels and induces a persistent depolarization -one of the most potent toxins
43
botulinum toxin
cleaves components of SNARE -VAMP and SNAP proteins stop vesicular fusion
44
curare alkaloids
non-depolarizing competitive nAChR antagonist
45
succinylcholine
depolarizing nAChR agonist only acts on the Nm (skeletal muscle) nAChR -but acts as antagonist (tires out receptor)
46
neuromuscular blocking drugs
used for causing muscle paralysis during anesthesia induction curare and succinylcholine
47
cholinesterase inhibitor
increase concentration of ACh at NMJ organophosphates -activate smooth and skeletal muscles used in lower concentration therapeutically
48
therapeutic use of low concentration cholinesterase inhibitor?
dementia, alzheimers, parkinsons, myasthenia gravis, reversal of neuromuscular blockade during anesthesia
49
myasthenia gravis
decreased in nAChR on surface of cell -cholinesterase inhibitor will increase ACh to activate the decreased nAChR
50
tetrodotoxin
also affects sodium channels on muscle cells (inhibits APs)
51
dantrolene
inhibits ryanodine receptor in SR - blocks release of Ca2+ - no contraction
52
clinical use of dantrolene?
malignant hyperthermia, spasticity with upper motor neurons
53
uptake of choline
rate limiting step
54
endoytosis of vesicles
facilitated by clathrin
55
tertodotixin
puffer fish toxin blocks axonal conduction -blocks Na+ channels (not used clinically)
56
local anesthetics
block neuronal conduction -inhibits Na+ channels used for pain control during variety of clinical procedures
57
botulinum
cleaves components of core SNARE complex -prevents ACh release ``` treatments: -strabismus -blepharosmam with dystonia -cervical dystonia -wrinkles of face - ```
58
curare alkaloids
non-depolarizing competitive nAChR antagonist during anesthesia to relax skeletal muscle
59
succinylcholine
neuromuscular blocking drug binds to nAChR - acts as an agonust -continued depolarization leads to receptor blockade and paralysis
60
dantroleine
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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