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Cell physiology and pharmacology > Lecture 10- The Neuromuscular junction > Flashcards

Lecture 10- The Neuromuscular junction Flashcards

1
Q

The higher the frequency of AP, the more

A

ca2+ entry into presynaptic bouton

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2
Q

the more ca2+ entry into presynaptic bouton….

A

more NT released

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3
Q

the more NT released into the synaptic cleft…

A

the more likely to initiate AP above threshold in post synaptic neurone

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4
Q

outline how calcium promotes exocytosis of NT

A
  1. Action potential
  2. Opens voltage gated Ca2+ channels
  3. Ca2+ influx
  4. Increased [Ca2+]i
  5. Ca2+ binds to synaptotagmins
  6. NT vesicles brought close to the membrane
  7. Vesicles bind to Snare complex and makes fusion pore
  8. Content of vesicle diffuse into the synaptic cleft
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5
Q

voltage gated calcium channel has a similar structure to

A

NaV

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6
Q

calcium channels are

A

diverse- many different isoforms

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7
Q

name the 5 different types of calcium channel

A

L- type- muscle, neurones, lung

Blocked by DHP (dihydropyridines e.g. Nifedipine

N- type- neurone

P/Q- type- neurone

R- type- neurone

T- type- neurone, heart

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8
Q

properties of calcium channel

A
  • CaV activate more slowly than Nav
  • Can be activated and inactivated- slower than Na+ channel
  • Inactivation is Ca2+ dependent.
  • Increased intracellular [Ca2+] leads to inactivation of Ca2+ channels
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9
Q

the NMJ is the

A

synapse between nerve and skeletal muscle fibres

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10
Q

types of voltage gated channels in the nerve terminal

A

voltage gates Na+, K+ and Ca2+

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11
Q

when the membrane depolarises what happens to voltage gated calcium channels

A

calcium channels open causing influx

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12
Q

what is the motor endplarte

A

keletal muscle surface

  • junctional folds increase the number of AChR –> increasing depolarisation
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13
Q

what degrades Ach in the synapse

A

AChesterase

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14
Q

what produces ACh

A

ACh transferase

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15
Q

outline synaptic transmission at the NMJ

A
  1. ACh from vesicle diffuses across the synaptic cleft and binds to Nicotinic (ionotropic) acetylcholine receptor (nAChR)
  2. Ligand gated receptor
  3. When 2 Ach binds to nAChR it allows ion sodium to enter the cell– depolarisation (end plate potential)
  4. Brief depolarisation of end plate will activate adjacent sodium channels due to local spread of charge causing muscle AP
  5. AP then initiates contraction of skeletal muscle fibre via excitation contraction coupling
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16
Q

NMJ and amazonian poison

A

Amazonian people use a poison called curare to hunt.

  • Curare causes paralysis – easy to kill
  • Blocks transmission at NMJ
  • Eating curare is ok
17
Q

myasthenia gravis is an

A

autoimmine disease, where antibodies target nAChR on the postsynaptic membrane on skeletal muscle

  • a reduction in 30% of nAChR is sufficient to give symptoms
18
Q
A
19
Q

how do the antibodies destory the nAChR

A

by complement mediated lysis and receptor degradation

20
Q

degradation of nAChR on the motor end plate causes

A

Endplate potentials are reduced in amplitude leading to muscle weakness and fatigue

21
Q

what tes tis used to diagnose MG

A

endrophonium test

22
Q

endrophonium test

A
  1. Facial weakness is provided by repeated facial movements (left)
  2. Edrophonium chloride (short acting anticholinesterase- increases conc of ACh in synaptic cleft) given via intravenous injection
23
Q

positive endrophonium test

A

facial weakness rapdily relieved

24
Q

where should edrophonium test be carried out

A

Test should always be done in a hospital where there are resuscitation facilities and with a drawn up syringe of atropine (a muscarinic receptor antagonist) present

25
Q

organophosphate poisoning

A
  • Organophosphates are used as insecticides (e.g. parathion, dimethoate)
    • Accidental or self inflicted poisoning
  • More powerful ones have been developed against nerve agents used in war or terrorism
26
Q

name some organophosphate agents (synthetic) which have been developed against nerve agents used in war or terrorism

A

sarin

novickok

27
Q

how do organophosphates cause poisoning

A

1) Inhibitors that form a stable irreversible covalent bond to ACh esterase
2) Recovery from poisoning may take weeks as synthesis of

new acetylcholinesterase enzymes are needed

28
Q

ACh binds to both

A

nicotinic (somatic NS, ganglions) and muscarinic (parasympathetic) receptors

29
Q

muscarinic receptors are

A

metabotropic

  • slow
  • GPCRs- second messenger cascade
30
Q

how many types of mAChR

A

M1- exc

M2- exc

M3- inhib

M4- inhib

M5- exc

31
Q

nAChR

A

Fast, Ligand-gated

Cholinergic, Ionotropic

Coupled to ion channels

Excitatory receptors

Two types

N1

N2

Cell physiology and pharmacology (20 decks)

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