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MSK SM > Physiology of the Neuromuscular Junction > Flashcards

Physiology of the Neuromuscular Junction Flashcards

1
Q

What type of movement does skeletal muscle mediate

A

Voluntary movement

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2
Q

What innervated skeletal muscles

A

Motor neurones with myelinated axons and cell bodies in the spinal cord or brain stem

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3
Q

Each unmyelinated branch of a motor neurone axon innervates how many skeletal muscle cells within a muscle

A

One

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4
Q

What is a motor unit

A

The neurone and the number of fibres that it innervates

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5
Q

What forms a chemical synapse with the muscle membrane at the neuromuscular junction

A

Individual branches which have further divided into multiple fine branches, each ending in a terminal bouton

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6
Q

What causes the release of the neurotransmitter acetylcholine?

A

Action potentials that arise in the cell body conduct via the axon to the boutons causing the release

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7
Q

Where does the presynaptic terminal (bouton) synapse at?

A

The endplate region of skeletal muscle fibres

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8
Q

What are the 4 key features of the skeletal Neuromuscular junction

A
  1. the terminal bouton (and surrounding Schwann cell
  2. synaptic vesicles
  3. the synaptic cleft
  4. the end palte region of the muscle cell membrane (sarcolemma)
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9
Q

Where are nicotinic ACh receptors located

A

At regions of the junctional folds that face the active zones

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10
Q

What is contained in the synaptic vesicles

A

A high concentration of ACh

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11
Q

How large is the synaptic cleft

A

Very narrow

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12
Q

Describe the 5 steps involved in the synaptic transmission at the skeletal neuromuscular junction

A
  1. synthesis of Neurotransmitter
  2. Storage of neurotransmitter
  3. release of Neurotransmitter under control of Ca+
  4. Receptor activation
  5. Transmitter inactivation - mediated by Ach esterase
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13
Q

How is choline transported into the terminal

A

By the choline transporter - this requires energy

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14
Q

What concentrates ACh in the vesicles

A

The vesicular ACh transporter

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15
Q

What happens when the Action Potential arrives at the terminal

A

Causes depolarisation and the opening of voltage activated Ca2+ channels. This allows Ca2+ entry to the terminal

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16
Q

What does Ca2+ cause the vesicles to do

A

Fuse with the presynaptic membrane
This allows ACh to diffuse into the synaptic cleft to activate post synaptic nicotinic ACh receptors in the endplate region

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17
Q

In the post synaptic process, what does ACh activate

A

Nicotinic ACh receptors located at the muscle end plate

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18
Q

How are Nicotinic ACh receptors assembled

A

As a pentamer of glycoprotein subunits that surround a central, cation selective pore. (5 M2 helicesmake this pore)

19
Q

What does the pore contain

A

A gate that is closed in the absence of ACh but open when two molecules of ACh bind to the exterior of the receptor

20
Q

What happens when the gate is open

A

Na enters the muscle cell whilst K exits simultaneously through many receptors at the end plate

21
Q

Why is influx of Na greater than the efflux of K+

A

Because of the driving force for Na being greater than that for K+ at resting membrane

22
Q

What causes the generation of the end plate potential

A

The depolarisation due to the greater influx of Na compared to that of the efflux of K+

23
Q

What is a miniature endplate potential

A

The electrical response to one quantum of transmitter, due to the activation of nicotinic ACh receptors at the endplate

24
Q

How is a contraction initiated

A

When an end-plate potential exceeds threshold triggers and an all or none propogated action potential will initiate contraction

25
Q

What type of response is the EPP

A

A graded response

26
Q

What causes a twitch of the muscle

A

Normally one action potential in the motor nerve triggers one action potential in the muscle (one to one coupling)

27
Q

Describe the way in which action potentials spread in skeletal muscle

A

They are regenerative - as soon as 1 opens, adjacent ones are reached and rapid interaction occurs

28
Q

What happens when an action potential arrives at the T tubule

A

It triggers release of Ca2+ from the SR which in turn causes contraction by interacting with troponin associated with the myofibrils

29
Q

What is the result of hydrolysis of ACh by acetylcholinesterase

A

Rapid termination of the neuromuscular transmission

30
Q

What happens to the acetate when ACh is hydrolysed

A

It diffuses from the synaptic cleft

31
Q

What is an important target of some therapeutic agents and also some insecticides and nerve gases used in warfare

A

Aceytlcholinesterase

32
Q

What are some of the symptoms of Neuromyotonia (Isaac’s syndrome)

A

Multiple disorders of skeletal muscle function including cramps, stiffness, slow relaxation and muscle twitches

33
Q

What is the drug treatment for Neuromyotonia

A

Anti-convulsants (carbamazepine, phenytoin) which block voltage activated Na+ channels

34
Q

What is Lamber-Eaton Myasthenic Sydrome characterised by

A

Muscle weakness in the limbs, very rare and associated with small cell carcinoma of the lung

35
Q

What is the origin of LEMS

A

Autoimmune - antibodies against voltage activated Ca2+ channels in the motor neurone terminal result in reduced Ca2+ entry in response to depolarisation and hence reduced vesicular released of ACh

36
Q

WHat is the drug treatment for LEMS

A

Anticholinesterases (pyridostigmine) and potassium channel blockers which increase the concentration of ACh in the synaptic cleft

37
Q

What is Myasthenia Gravis characterised by

A

Progressively increasing muscle weakness during periods of activity
Often weakness of the eye and eyelid muscles is a presenting feature

38
Q

What is the drug treatment for Myasthenia Gravis

A

Anticholinesterased (edrophonium for diagnosis and pyridostigmine for treatment)
Also use an immunosuppressant agent (azathioprine)

39
Q

What is Botulinum Toxin

A

An extremely potent exotoxin toxin (related to tetanus and diptheria toxins) that act at motor neurone terminals to rreversibly inhibit ACh release

40
Q

What does Botulinum Toxin do when it enters the presynaptic nerve terminal?

A

Enzymatically mofidies proteins involved in the docking of vesicles containing ACh

41
Q

What is the death rate like in Botulinum Toxin

A

High - recovery takes several weeks - drugs that block acetylcholinesterase are ineffective as therapy

42
Q

How is botulinum haemaglutin complex administered

A

By intramuscular injection to treat overactive muscles (e.g. extraocular muscles)

43
Q

What do curare-like compounds do?

A

They Interfere with the postsynaptic action of acetylcholine by acting as competitive antagonists of the nicotinic ACh receptor
Reduce the amplitude of the endplate potential to below the threshold for muscle fibre action potential generation

44
Q

Why are curare-like compounds used clinically

A

to induce reversible muscle paralysis in certain types of surgery

MSK SM (42 decks)

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