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MSK1 > Physio of the NMJ > Flashcards

Physio of the NMJ Flashcards

1
Q

What enzyme causes the creation of acetylcholine?

A

Choline acetyltransferase (ChAT) combines acetyl coa from within the axon terminal with choline that was from the outside of the cell that came in via choline receptors

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2
Q

What do patients with alzheimers have less of?

A

Choline acetyltransferase

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3
Q

What are the VAMPS that are housed on the synaptic vesicle?

A

Synaptobrevin and synaptotaxin

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4
Q

What are the SNAPS that are housed on the axon membrane?

A

SNAP25 and Syntaxin

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5
Q

What is needed for the creation of the SNARE complex that fuses the synaptic vesicle with the plasma membrane of the axon?

A

Calcium influx that is caused from the sodium influx of the AP

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6
Q

What is responsible for the inhibition of acetylcholine in the synaptic cleft?

A

Acetylcholinesterase (AchE) - an enzyme that destroys ACH and breaks it up into acetyl coa and choline that is recycled

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7
Q

What receptors does ACH bind to on the muscle fiber?

A

Nicotinic acetylcholine receptors (NAchR)

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8
Q

What is the action of NAchRs?

A

Allow a lot of sodium into the cell and allow some potassium out of the cell

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9
Q

As the depolarization travels down the T-tubule, it reaches receptors… what are those receptors?

A

Dihydropyradine receptors that are attached to ryanodine receptors on the terminal cisternae

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10
Q

What is the action of the dihydropyradine receptors?

A

They pull off the ryanodine receptors and allow calcium out of the terminal cisternae so it can bind to troponin and allow sarcomere/muscle contraction

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11
Q

What creates the resting membrane potential?

A

Sodium/potassium pump (pumps 2 K in and 3 Na out) and leaky K+ channels that allow potassium to leave the cell and follow conc. gradient which results in a more negative cell

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12
Q

What inhibits the choline receptors on the axon?

A

Hemicholinium

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13
Q

What inhibits ACH from being transported into synaptic vesicles?

A

Vesamicol

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14
Q

What destroys the SNARE complex and does not allow synaptic vesicle fusion?

A

Botulinum toxin

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15
Q

What are the agents that affect the nerve AP?

A

Tetrodoxin and local anesthetics

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16
Q

Tetrodoxin

A

Inhibits voltage gated sodium channels and blocks axonal conduction “pufferfish poison”
symptoms = weakness, dizziness, paralysis, death

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17
Q

Local anesthetics

A

Such as lidocaine, inhibit voltage gated sodium channels and inhibit axonal conduction, used for pain control

18
Q

What are the agents that block vesicular ACH release?

A

Botulinum toxin and tetanus toxin

19
Q

Botulinum toxin

A

Cleaves SNARE complex which prevents ACH release from synaptic vesicle; sound on fruits, veggies, seafood
Symptoms: blurred vision, nausea, vomiting, diarrhea;
Clinically - used to limit face wrinkles and stop migraines

20
Q

Tetanus toxin

A

Found in soil; Targets synaptobrevin and then transported retroaxonally to spinal cord where it inhibits spinal interneurons that serve to relax skeletal muscle
Symptoms: muscle spasms, trismus (lockjaw), stiff neck, rigid abdomen, autonomic overactivity - tachycardia, sweats

21
Q

What are the agents that affect depolarization?

A

Agonists and Antagonists of NAchR, curare alkaloids, succinylcholine

22
Q

What do agonists do?

A

Bind to receptor and open it

23
Q

What do antagonists do?

A

Bind to receptor and keep it closed

24
Q

Curare alkaloids : d-tubocurarine

A

Competes with ACH to bind to NAchR, blocks opening of receptor and leads to muscle flaccid paralysis

  • Used to relax muscle in surgery and overcome by increased ACH
  • Keeps gates closed on receptor
25
Q

Succinylcholine

A

Depolarizing neuromuscular blocker; binds to NAchR and initially causes depolarization but leads to receptor blockade and paralysis

  • Effects reversed with time
  • Binds and opens receptor but then blocks it
26
Q

What are the agents that inhibit AchE?

A

Acetylcholinesterase inhibitors

27
Q

Acetylcholinesterase inhibitors

A

Block enzymatic activity which results in a high concentrations of ACH at the NMJ

28
Q

What are the clinical uses of AchE inhibitors?

A

Used to treat dementia in alzheimers/parkinson’s pts, myasthenia gravis, nerve gas, organophosphate pesticide, reversal of neuromuscular blockade during anesthesia

29
Q

What are the agents that affect muscle contraction?

A

Dantrolene

30
Q

Dantrolene

A

Inhibits ryanodine receptors and prevents calcium release so no muscle contraction
- Clinically used to treat malignant hyperthermia and spasticity

31
Q

Site where electrical signal from one excitable cell is communicated with another

A

Synaptic transmission

32
Q

What are the 2 types of synaptic transmission?

A

Electrical (heart) and chemical (uses NT)

33
Q

How many innervations from a presynaptic cell does the muscle fiber receive?

A

1

34
Q

What causes muscles to lose tension despite continuing stimuli?

A

Fatigue

35
Q

What are the 2 types of fatigue?

A

Peripheral (requires availability of ATP) and central (Brought on by buildup of byproducts from contraction such as lactic acid and H+)

36
Q

What are the 3 fiber types?

A

Slow twitch oxidative, fast twitch glycolytic and fast twitch oxidative

37
Q

What energy does slow twitch oxidative use?

A

O2

38
Q

What energy does fast twitch glycolytic use?

A

Phosphocreatine and glucose

39
Q

What does the force of contraction depend on?

A

Starting length of sarcomere and how rapidly a fiber is stimulated by a nerve

40
Q

What is tetanus?

A

Overlap of muscle twitches such that complete relaxation between them is not achieved

41
Q

Neurons that innervate more fibers will generate a smaller or greater force?

A

GREATER

42
Q

What happens to a muscle with glycolytic fibers?

A

Generates more force but fatigues quickly

MSK1 (29 decks)

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