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MSK 2 > Pharmacology - NMJ > Flashcards

Pharmacology - NMJ Flashcards

1
Q

Steps involved in NMJ neurotransmission

A
  1. Axonal conduction
  2. Junctions transmission
  3. ACH signaling
  4. Muscle contraction
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2
Q

Junctions transmission

A
  1. ACH synthesis
  2. ACH storage
  3. ACH release
  4. ACH destruction
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3
Q

Membrane channel that transports choline into cell

A

Choline transporter

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4
Q

Enzyme that combine acetyl coenzyme A (AcCoA) and choline to form ACH

A

Choline acetyltransferase (ChAT)

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5
Q

Choline transporter inhibitor

A

Hemicholinium

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6
Q

Opens upon depolarization and allows Ca2+ to enter the cell

A

Voltage-gated Ca2+ channels

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7
Q

What does release of Ca2+ via voltage-gated Ca2+ channels promote?

A

Vesicle membrane fusion

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8
Q

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

A

VAMP and SNAPs

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9
Q

What does acetylcholinesterase (AChE) cleave acetylcholine into?

A

Choline and acetate

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10
Q

What happens to the choline produced by breakdown of ACh?

A

Recycled back into motor neuron via choline transporter

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11
Q

What process occurs are the nerve terminal to replenish number of available vesicles?

A

Endocytosis

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12
Q

2 subsets of acetylcholine receptors

A
  • nicotonic acetylcholine receptors (nAChRs)

- muscarinic (mChRs)

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13
Q
  • activated by ACh and nicotine
  • ligand-gated ion channel (Na+)
  • pre and post-junctions
  • at NMJ: Na+ increase causes muscle AP
A

NAChRs

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14
Q
  • activated by ACh and muscadine
  • GPCR
  • pre and post-junctions
  • NOT located at skeletal NMJ
A

MAChR

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15
Q

Where are mAChRs found?

A
  • smooth muscle

- cardiac muscle

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16
Q

Function of nAChR and mAChr in skeletal muscle and smooth muscle (respectively)

A

Contraction

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17
Q

Function of mAChR in cardiac muscle

A

Decreased HR, conduction velocity, contraction

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18
Q

Number of mAChR subtypes in mammals

A

5 (M1-M5)

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19
Q

Metabotropic

A

Activation leads to series of intracellular events triggered by second messengers

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20
Q

Ionotropic

A

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

21
Q

Describe selectivity of ions

A

Based on charge of amino acid

Ex: negative charge within pore of nAChR = allows positive ions to pass

22
Q

Molecular response of all types of nAChRs

A

Increased cation permeability (Na+ and K+; Ca2+ in CNS)

23
Q

Agonists of skeletal muscle (Nm)

A

ACh
Nicotine
Succinylcholine

24
Q

Antagonists of skeletal muscle (Nm)

A
  • d-tubocurarine
  • atracurium
  • vecuronium
  • pancuronium
25
Q

Antagonists of peripheral neuronal (Na) and central neuronal receptors

A

Mecamylamine

26
Q

Synaptic location for peripheral neuronal (Nn) vs. central neuronal

A
  • peripheral neuronal: autonomic ganglia & adrenal medulla
  • central neuronal: CNS
27
Q

Events at the NMJ

A
  1. AP propagated to terminal button
  2. AP triggers opening of voltage-gated Ca2+ channels
  3. Ca2+ triggers release of ACh from vesicles
  4. ACh diffuses across synaptic cleft and activates nAChRs
  5. NAChRs open > large include of Na+ compared to small effluent K+
  6. Local current flows b/w de polarized end plate and adjacent membrane
  7. Local flow opens voltage-gated Na+ channels
  8. Influx of Na+ initiates an AP which propagates throughout muscle fiber
  9. ACh is destroyed by ACHE, terminated cells response
28
Q

Tetrodotoxin, batrachotoxin, local anesthetics

A

Block nerve AP

29
Q

Hemicholinium, botulinum toxin, procaine, Mg2+, 4-aminopyridine, lack of Ca2+

A

Block vesicular acetylcholine release

30
Q

Excess of Ca2+

A

Promotes vesicular acetylcholine release

31
Q

Curare alkaloids and snake alpha-toxins

A

Block depolarization (EPP) (increased permeability to Na+ and K+)

32
Q

Succinylcholine and decamethonium

A

Depolarization and phase II block

33
Q

Cholinesterase inhibitors

A

Block hydrolysis of acetylcholine by cholinesterase

34
Q

Ca2+ and veratridine

A

Enhance muscle AP

35
Q

Quinine and tetrodotoxin

A

Block muscle AP

36
Q

Metabolic poisons, lack of Ca2+, procaine, dantrolene

A

Block muscle contraction

37
Q
  • puffer fish poison
  • inhibition of voltage-gated Na+ channels block axonal conduction
  • weakness, dizziness, paresthesia of face and extremities, loss of reflexes, hypotension, general paralysis, death from respiratory failure and hypotension
A

Tetrodotoxin

38
Q
  • inhibition of voltage-gated Na+ channels inhibition axonal conduction
  • used for pain control during clinical procedures
  • ex: lidocaine, bupivicaine, procaine
A

Local anesthetics

39
Q
  • cleaves components of core SNARE complex involved in exocytosis, preventing release of ACh
  • caused by Clostridium botulinum (heterogenous group of gram-positive, rod-shaped, sport-forming, obligate anaerobic bacteria; found on vegetabless, fruits, seafood, etc.)
  • classically described as cute onset of bilateral cranial neuropathies associated with symmetric descending weakness
  • used with temporary improvement in appearance of lines/wrinkles of face, prophylaxis of chronic migraine headache
A

Botulinum toxin

40
Q

Nervous system disorder characterized by muscle spasms caused by Clostridium tetani (toxin-producing anaerobes) found in soil

A

Tetanus

41
Q
  • block fusion of synaptic vesicles by targeting synaptobrevin
  • after blinding to presynaptic membrane of NMJ, tetanus toxin is internalized and transported retroaxonally to SC
  • spastic paralysis caused by toxins actions on spinal inhibitory interneurons, blocking release of inhibitory NT that serve to relax contracted muscle by inhibiting excitatory motor neurons
A

Tetanus toxin

42
Q

Spastic paralysis with symptoms that include trismus, autonomic overactivity, stiff neck, board-like rigid abdomen, opisthotonos, dysphasia

A

Symptoms of tetanus

43
Q

Activate receptor to signal as a direct result of binding to it

A

Agonist

44
Q

Bind to receptors but do not activate generation of signal

A

Antagonists

45
Q
  • Competes with ACh for the nAChR on the motor end plate > decrease size of EPP
  • inhibits ACh binding to nAChR > flaccid paralysis of skeletal muscle
  • used during anesthesia to relax skeletal muscle
  • paralysis reversed by increasing ACh in the NMJ
A

Curare alkaloids (d-tubocurarine)

46
Q
  • depolarizing neuromuscular blocker that binds to skeletal muscle nAChRs and causes depolarization > continued depolarization leads to receptor blockade and paralysis
  • used as induction agent for anesthesia
  • paralysis reversed by termination of succinylcholine’s effects
A

Succinylcholine

47
Q
  • bind to AChE and block enzymatic activity
  • increase concentration of ACh at the NMJ
  • clinical uses: dementia (Alzheimer’s or Parkinson’s), myasthenia Travis, nerve gas and organophosphate pesticide exposure, reversal of neuromuscular blockade during anesthesia
A

Cholinesterase inhibitors

48
Q
  • inhibit RyR in the SR and blocks release of Ca2+

- clinical use: malignant hyperthermia, spasticity associated with upper motor neuron disorders

A

Dantrolene

49
Q

blocks the ACh vesicular transporter

A

Vesamicol

MSK 2 (12 decks)

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