NMJ Flashcards

1
Q

What is the NMJ?

A

specialised synapse between motor neurone (distal axons terminal) and muscle fibre membrane

allows for unidirectional chemical communication between peripheral nerve and muscle

main structures: presynaptic terminal, synaptic cleft, postsynaptic endplate region on muscle fibre

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2
Q

What is the bouton?

A

presynaptic terminal

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3
Q

What two structures can be found on muscle membrane?

A

ACh receptor

AChesterase (breakdown neurotransmitter)

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4
Q

What is the main NT for voluntary striated muscle?

A

ACh

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5
Q

What are the upper and lower motor neurones?

A

upper - originate in brain

lower - in brain stem to face
in spinal cord to arms, leg or trunk

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6
Q

What emerges through anterior and dorsal/posterior roots of spinal cord?

A

dorsal root - afferent/sensory neurones

anterior - efferent/motor neurones

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7
Q

What is located in the anterior horn?

A

efferent neurone cell bodies

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8
Q

Describe the important organisation of motor innervation of muscle fibres?

A

mixture of nerve fibres innervating mixture of muscle fibres
single muscle fibre only received innervation from branch of one neurone

injury - regrowth of nerve causes innervation from different nerves

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9
Q

Describe NMJ process?

A
  1. AP opens VGCCs causing Ca influx to motor end plate
  2. Stimulates exocytosis of vesicles
  3. ACh diffuses in cleft and binds to receptor-cation channel to open channel
  4. local currents flow from depolarised region and adjacent region to spread across muscle surface membrane
  5. ACh broken down the AChesterase
  6. Muscle fibre response to ACh stops
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10
Q

What are MEPPs?

A

at rest vesicles release ACh at very low rate causing miniature end-plate potentials

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11
Q

What is muscle made up of?

A

Fasciculi of muscle fibres surrounded by connective tissue

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12
Q

What is a myofibre?

A

covered by sarcolemma and made of myofibrils
T tubules tunnel into sarcoplasm to activate individual proteins (contains mitochondria and myoglobin)
network of fluid filled tubules (SR)

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13
Q

What are myofibrils?

A

1-2 micrometre diameter
extend along myofibres
made of actin and myosin
striated

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14
Q

What generates more force?

A

lengthening of muscle fibre

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15
Q

Concentric and eccentric muscle contraction?

A

Concentric - shorten, thereby generating force

Eccentric - elongate in response to a greater opposing force

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16
Q

What separated sarcomeres?

A

Z discs

17
Q

What is the dark band?

A

A band

thick myosin filament

18
Q

What is the light band?

A

I band

think actin filament

19
Q

How are A and I bands named?

A

effect on polarised light

20
Q

What changes and stay same in contraction?

A

distance between Z discs decreases
A band same length
H zone narrowed/dissappeared
I band shorter

21
Q

What is the function of the invaginations down into muscle?

A
  1. AP propagates along surface membrane into T tubules
  2. DHP receptor in membrane senses voltage change and changes shape to link to RyR and open Ca channel on SR membrane
  3. Ca released into sarcoplasm
  4. Ca binds to troponin and tropomyosin moved so crossbridges attach to actin
  5. Ca actively transported back to SR continuously while AP continue but ATP
  6. Ca dissociates from troponin when free Ca declines (no more released from SR) and tropomyosin prevents new crossbridge attachment - ACTIVE FORCE DECREASE DUE TO NET CROSSBRIDGE DETACHMENT
22
Q

What is the consequence of NMJ function affecting disorders?

A

cause muscle weakness

23
Q

What is botulinum toxin?

BOTULISM

A

causes irreversible disruption in stimulation-induced ACh release by PreS nerve terminal

no muscle effect

24
Q

What is myasthenia gravis?

A

autoimmune disorder - antibodies directed against ACh receptor

hereditary?

cause fatigable weakness (more pronounced with repetition), droop eyelids, cannot have face expression easily
ocular/bulbar (corticobulbar tract from cortex to brainstem to face muscles)/resp/limb muscle effects

EMG exam confirms diagnosis. presence of antibodies

remove antibodies in blood via plasma exchange to allow rapid improvement
prevent ACh degradation in synapse

25
Q

What is Lambert-Eaton myastenic syndrome?

A

autoimmune disease - antibodies directed against VGCC
failure of transmission at presynaptic site

administer ACh supplement

associated with lung cancer increased risk

26
Q

What is the function of SNARE protein?

A

mediate vesicle fusion, that is, the fusion of vesicles with their target membrane bound compartments (such as a lysosome)