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MSK exam 3 AP lower limb > Pharmacological view of NMJ > Flashcards

Pharmacological view of NMJ Flashcards

1
Q

cholinergic neuron?

A

neurotransmitter is ACh

can occur at NMJ and smooth muscle junction

neurons that are responsible for releasing acetylcholine in the brain or periphery

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2
Q

what does junctional transmission involve

A

Synthesis of acetylcholine (ACh)
Storage of ACh
Release of ACh
Destruction of ACh

almost all steps in this process can be inhibited by pharmacological agents

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3
Q

steps involved in NMJ neurotransmisison

A

Axonal conduciton
Junctional transmission
ACh signaling
Muscle contraction

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4
Q

what are nicotinic ACh Receptors

A

these are in subneural clefts that when activated lead to muscle contraction

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5
Q

ACh synthesis key players

A

choline transporter

choline acetyltransferase

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6
Q

what does choline transporter do?

A

transports choline into the cell

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7
Q

what does choline acetyltransferase do?

A

ChAT

enzyme that combines acetyle coA (AcCoA) and choline to form ACh

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8
Q

what do patients with Alzheimer’s disease have?

A

reduced cerebral production of ChAT
the enzyme that makes ACh

therapeutic is to increase levels of ACh to make up for decrease

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9
Q

what is ACh vesicular transporter ?

A

ATP dependent transporter that immediately shuttles ACh into storage vesicles after ACh synthesis

responsible for ACh storage

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10
Q

how many vesicles may a motor nerve terminal contain

A

over 300 K

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11
Q

ACH release happens when?

A

AP reaches the end of the neuron
voltage gated Ca channels open up Ca enters cell

Ca promotes vesicle membrane fusion

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

forms snare complex

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12
Q

Botulin/Botox does what?

A

can’t have fusion of vesicle and don’t have subsequent release of ACh

don’t have muscle contraction, basically having paralysis

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13
Q

Acetylcholinesterase

A

AChE

enzyme that cleaves ACh into choline and acetate

choline is recycled back into the motor neuron via the choline receptor

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14
Q

muscarinic Ach receptors

A

found on cardiac cells and smooth muscle

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15
Q

nicotinic ACh receptors

A

most important with the skeletal muscle contraction process

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16
Q

nicotinic ACh receptors

A

Activated by ACh and nicotine

Ligand-gated ion channel (Na+)
(sodium flows in upon activation–> leading to muscle AP) so very FAST

Pre- and postjunctional

NMJ: Na+ increase causes muscle action potential

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17
Q

mAChRs

A

ated by ACh and muscarine

G-protein coupled receptor

Pre- and postjunctional

NOT located at skeletal NMJ

18
Q

tissue location of nA ChR and mAChR

A

N–> skeletal muscle
- when activated cause contraction

M—> smooth muscle , cardiac muscle (SA node, AV node, Atrium, Ventricle)
-when activated cause contraction

19
Q

agonists of nAChR (cause receptor to be activated)

A

acetylcholine

Nicotine

20
Q

agonists of mAChR

A

acetylcholine

muscarine

21
Q

what are the functions of mAChR

A

Contraction of smooth muscle

cardiac--> 
↓ HR
↓ conduction velocity
↓ contraction
Slight 
↓ contraction
22
Q

parasympathetic

A

aceytlcholine activating muscarnic receptors

23
Q

sympathetic

A

fight or flight, nicotinic???

24
Q

what type of channels are nAChR’s and what do they allow?

A

ligand gated ion channels

have two binding sites for ACh

Ligand-gated ion channels allow ions to pass through the channel pore when activated

IONOTROPIC

25
Q

why are the nAChR’s receptors made up of 4-5 subunits

A

b/c when you have a drug you only want the drug that will affect a certain receptor on a specific type of cell . allows for selectivity of drugs !!

so skeletal muscle nAChR’s are different in skeletal muscle than they are in neuronal receptors

26
Q

Nm (skeletal muscle) receptor subtype of nAChR’s

A

activated causes excitation of skeletal muscle

main location is skeletal neuromuscular junction (postjunctional)

allows sodium ions to come in (increased cation permeability)

agonists ACh, nicotine, Succinyl-choline

27
Q

nAChR postjunctional activation involves what?

A

Two ACh molecules bind to both binding sites

Positively charged ions (Na+, K+, Ca2+) pass through the channel

The muscle cell is depolarized and an action potential is initiated

28
Q

nAChR ‘s prejunctional activation involves what?

A

when these are activated it allows for more vesicles to move toward the synaptic membrane

mobilization of additional ACh for subsequent release

29
Q

tetrodotoxin

A

puffer fish): inhibition of voltage-gated Na+ channels prevents axonal conduction

if you inhibit these you can’t get action potential going down the neuron and you become paralyzed

can cause diaphragm paralysis and cannot breath

expensive in sushi b/c the chef has to prepare it correctly

30
Q

local anesthetics

A

inhibition of voltage-gated Na channels prevents axonal conduction

blocks skeletal muscle from being activated

blocks pain going back up to brain

31
Q

Batrachotoxin

A

(poison dart frog): causes an increase in permeability of Na+ channels and induces a persistent depolarization

One of the most potent toxins

32
Q

botulinum toxin

A

cleaves components of the SNARE complex (VAMP/SNAP proteins)

agent that affects vesicular ACh release

33
Q

agents that affect depolarization

A

Curare alkaloids
Succinylcholine
Snake alpha toxins

Neuromuscular blocking agents

Used for causing muscle paralysis during anesthesia induction (surgery)

34
Q

Curare alkaloids

A

nondepolarizing competitive nAChR antagonists

35
Q

succinylcholine

A

depolarizing nAChR agonist

36
Q

snake alpha toxins

A

competitive irreversible inhibitor of nAChR’s

37
Q

agents that inhibit AChE

A

Cholinesterase inhibitors

Bind to AChE and block its enzymatic activity

Increase the concentration of ACh at the NMJ

Clinical uses include dementia associated with Alzheimer or Parkinson disease, myasthenia gravis, nerve gas and organophosphate pesticide exposure, reversal of neuromuscular blockade during anesthesia

these people who have been exposed to this will have urinated themselves, tearing/watery eyes
can lead to paralysis because of the sustained activation

38
Q

myasthenia gravis treatment?

A

give patient something that will give them more acetylcholine

give them cholinesterase inhibitor

39
Q

Tetrodotoxin

A

blocks the outer mouth of Na+ channels and inhibits action potentials

40
Q

Dantrolene

A

Inhibits ryanodine receptors in the sarcoplamic reticulum and blocks release of Ca2+

Clinical uses include malignant hyperthermia, spasticity associated with upper motor neuron disorders

agent that affects muscle contraction

41
Q

extreme and profound activation of skeletal muscle

A

malignant hypothermia

how to treat? dantrolene

MSK exam 3 AP lower limb (15 decks)

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