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MSK Exam 2 > Neuropharm > Flashcards

Neuropharm Flashcards

1
Q

ACh Synthesis

A
  1. Choline transporter

2. Choline acetyltransferase (ChAT)

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2
Q

Choline transporter

A

Choline transporters will bring [choline] into the cell.

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3
Q

Choline acetyltransferase

A

[choline]+[acetyl Co-A] –> Acetylcholine

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4
Q

Alzheimers patients have a increased/decreased amount ChAt

A

decreased

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5
Q

After ACh is made, how do we move it into vesicles?

A

ACh vesicular transporter

an ATP dependent transporter that moves ACh into storage vesicles.

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6
Q

How do we release ACh

A

VGCa2+ channels will allow the influx of Ca2+ when depolarized, causing the vesicles to move to the membrane.

[VAMPs and SNAPS] are proteins that cause the vesicle to fuse with the plasma membrane and release ACh.

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7
Q

ACh destruction

A

Acetylcholinesterase (ACheE) breaks down ACh into [choline and esterase]

Choline transporter brings the choline back into the pre-motor neuron.

Endocytosis occurs at the nerve terminal, to replenish number of vesicles.

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8
Q

ACh signaling

A

ACh can then activate

  1. nAChR
  2. mAChR
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9
Q

nAChR

Activated by:
Type of receptor:
Location:
Effect:

A
  • Activated by nicotine and ACh
  • Ligand-gated ion receptor
  • Located on the pre and post junctions

Effect: Increase in Na+ will result in a muscle AP.

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10
Q

mAChR

Activated by:
Type of receptor:
Location:

A
  • Muscarine and ACh
  • GPCR
  • Pre and post junctional
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11
Q

Where are nAChR located

A

skeletal m

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12
Q

Where are mAChR located

A

Smooth muscle and cardiac (ANS)

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13
Q

Binding of ACh to skeletal m nAChR causes what?

A

Contraction

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14
Q

Binding of ACh to smooth muscle mAChR causes what?

A

Contraction

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15
Q

Binding of ACh to cardiac muscle mAChR causes what?

A

Decreased HR, conduction velocity, decreased contraction and slight decreased contraction of atrium and ventricle

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16
Q

What type of receptors are mAChRs?

A

GCPRs that span the membrane 7 times.

Activate intracellular events via by second messengers.

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17
Q

How many subtypes are there of mAChRs?

A

5

M1-M5

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18
Q

Effects of mAChRs are seen in ______

A

seconds

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19
Q

What type of receptors are nAChRs?

A

Ligand-gated ion channels.

When activated, they allow ions to pass through.

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20
Q

Effects of nAChRs are seen in _______

A

miliseconds. They are the fastest synaptic events in the NS.

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21
Q

How do we determine what ions pass through the ligand- gated ion channel?

A

The ion is determined by the amino acids that line the pore of the channel.

+ AA will allow - charged ions to pass through.

  • AA will allow + charged ions to pass through.
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22
Q

What AA line nAChRs and what ions can pass through?

A
  • Aspartic acid and glutamic acid line the pore of the channel ( - charged)
  • Thus, they allow [Na+, Ca2+, K+]
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23
Q

Skeletal muscle nAChR are located where?

A

skeletal neuromuscular junction (postjunctional)

24
Q

Skeletal muscle nAChR membrane response.

A

Excitatory, contract, due to increased permeability of Na+, K+.

25
Q

Skeletal muscle nAChR agonists

A
  1. ACh
  2. Nicotine
  3. Succinylcholine
26
Q

Skeletal muscle nAChR antagonists

A
  1. d-tubocurarine
  2. Atracurium
  3. Vecuronium
  4. Pancuronium
27
Q

Events at the NMJ (bring it all together)

A
  1. AP in the motor neuron propogates to the axon terminal.
  2. Presence of AP triggers the opening of VGCa2+ channels.
  3. Influx of Ca2+ triggers ACh to be released from the vesicles.
  4. ACh will diffuse across the synaptic cleft and bind to nAChR.
  5. nAChR’s opening will lead to a large influx of Na+ and a smaller influx of K+.
  6. Local current will flow in between the depolarized endplate and adjacent membrane, opening VGNa+ channels.
  7. Influx of AP initiates the AP, which propagates throughout the muscle fiber.
  8. Cells response is terminated by AChE.
28
Q

Tetrodotoxin

A
  • Puffer fish poison
  • Blocks the conduction of an AP by inhibiting VGNa+ channels.
  • Paralysis
29
Q

Local anesthetics such as lidocaine, bupivacaine, procaine

A
  • Block the conduction of an AP by inhibiting VGNa+ channels.
30
Q

Drugs that affect vesicular release of ACh

A
  1. Botulinum toxin

2. Tetanus toxin

31
Q

Botulinum toxin

Where is it found?
MOA:

A
  • Vegetables, fruits and seafood; soil and marine sediment

MOA: Cleaves the SNARE complex resp for exocytosis of ACh.

32
Q

Sx of botulinum toxin

A

Acute onset of bilateral cranial neuropathies assx with symmetric descending weakness.

  • Blurred vision is the only sensory deficit.
  • Foodborne botulism: NVD, abdominal pain, dry mouth
33
Q

Clinical use of botulinum toxin

A

botox, HA.

34
Q

Tetanus

A

NS disorder characterized by muscle spasms due to tetanus toxin, found in the soil.

35
Q

Tetanus toxin

MOA

A

Inhibits [synaptobrevin], which fuses synaptic vesicles to the membrane.

After it binds to the the presynaptic membrane of the NMJ, it is internalized and transported to the spinal cord.

36
Q

Neuromuscular junction is ______

A

cholinergic

37
Q

why are the effects of botulinum toxin and tetanus toxin different?

A

Both will prevent ACh from being released from the vesicle.

However, Tetanus toxin will be internalized and transported to the spinal cord. There it will have an effect on inhibitory interneuron by blocking the released of inhibitory NTs which relax contracted muscles by inhibiting excitatory MN.

38
Q

Tetanus toxin sx

A

spastic paralysis with

  1. tris mus (lock jaw)
  2. autonomic overactivity (restlessness, sweating, tachycardia), stiff neck
39
Q

Agents that affect depolarization

A

Neuromuscular blocking drugs

  1. Curare alkaloids (d-tubocurarine)
  2. Succinylcholine

They all cause paralysis.

40
Q

Neuromuscular blocking drugs types and actions

A

All neuromuscular blocking drugs cause paralysis. They can be agonists and antagonists of nAChR, which can both prevent synapatic transmission.

  1. Agonists will activate the R.
  2. Antagonists bind to the receptor but do not activate signal.
41
Q

D-tubocurarine description and MOA

A

curare alkaloid that is a neuromuscular blocking drug antagonist.

It competes for binding with ACh on the nAChR , decreasing the size of the EPP by not allowing depolarization.

42
Q

D-tubocurarine results

A

Leads to flacid paralysis of skeletal muscle. Thus, used during anesthesia.

43
Q

How can we reverse paralysis induced by d-tubocurarine?

A

Increasing ACh via AChE inhibitor

44
Q

What is d-tubocurarine called?

A

non-depolarizing competetiive nAChR antagonist

45
Q

Succinylcholine description and action

A

neuromuscular blocking drug (agonist)

Binds to nAChR and continues to depolarize the receptor, leading to receptor blockade and paralysis. If open for too long, the channel can be blocked by succinylcholine and make it unable to repolarize.

46
Q

Succinylcholine uses

A

induction agent for anesthesia

47
Q

How can we reverse paralysis induced by succinylcholine

A

Wait for effects to be over because its short-acting

48
Q

Name that DRUG: depolarizing neuromuscular blocking drug

A

Succinylcholine

Agonist

49
Q

Name that DRUG: Non-depolarizing neuromuscular blocking drug

A

Curare alkaloids ( d-tubocurarine)

Antagonist

50
Q

Cholinesterase inhibitors

A

Bind to AChE and block its enzymatic activity, increasing the ACh at the NMJ.

51
Q

Cholinesterase inhibitors clinical use

A
  1. dementia assx with Alzheimers or PArkinsons,
  2. myasthenia gravis
  3. nerve gas
  4. organophosphate pesticide
  5. Reverse anesthesia
52
Q

Agents that affect muscle contraction

A

Dantrolene

53
Q

Dantrolene

A

Inhibits ryanodine receptors and block the release of Ca2+

Used to treat [malignant hyperthermia], spasticity assx with upper motor neuron disorders

54
Q

What drugs affect the vesicular release of ACh?

A
  1. Botulinum toxin

2. Tetanus toxin

55
Q

What drugs prevent the conduction of an AP by blocking VGNa+ channels?

A
  1. Local anesthetics

2. Tetrodotoxin

MSK Exam 2 (23 decks)

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