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MSK lectures > Physiology of Skeletal Neuromuscular Junctions 03/10/18 > Flashcards

Physiology of Skeletal Neuromuscular Junctions 03/10/18 Flashcards

1
Q

What is the only voluntary muscle?

A

Skeletal

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2
Q

What innervates the skeletal muscle?

A

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

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3
Q

What does the motor neurone axon branch into near the muscle?

A

Unmyelinated branches

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4
Q

What does each unmyelinated branch innervate?

A

A single skeletal muscle fibre

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5
Q

What does each motor neurone branch end in?

A

Terminal bouton that forms a chemical synapse with the NMJ

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6
Q

What is the path of an action potential in a skeletal muscle fibre?

A

Arise in the cell body
Conducted via the axon
Causes release of ACh

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7
Q

What is the neurotranmitter for all skeletal muscle fibres and what receptor does it act of?

A

Acetylcholine

On Nicotinic receptors

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8
Q

What are the key features of a NMJ?

A

Terminal bouton (and surrounding schwann cell)
Synaptic vesicles
Synaptic cleft
End plate region of the muscle cell membrane

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9
Q

Where are synaptic vesicles and what do they contain?

A

Active ones

ACh

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10
Q

Where are nicotinic receptors present?

A

End plate region

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11
Q

Give and overview of synaptic transmission at the NMJ

A

Ach is stored in active vesicles, these build up
calcium causes this to be released
Activating the nicotinic receptor
The transmitter in inactivated

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12
Q

How is choline transported into the terminal?

A

Choline transport symport with Na+

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13
Q

What synthesises ACh and where does it occur?

A

Choline and acetyl coenzyme A
In the cytosol
By choline acetyltransferase

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14
Q

How is ACh concentrated into vesicles?

A

Vesicular ACh transporter

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15
Q

What does arrival of the action potiential at the terminal cause?

A

Depolariation and opening of voltage-activated Ca2+ channel allowing Ca entry to the terminal

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16
Q

What does calcium do to the vesicles?

A

They fuse with the presynaptic membrane (exocytosis) - Ach diffuses into the synaptic clept to activate post-synaptic nicotinic Ach receptors

17
Q

What is the arrangement of nicotinic Ach receptors?

A

Pentamer of glycoprotien subunits that surround a centeral cation

18
Q

What is contained in the centeral cation pore?

A

A gate that is closed in the absence of ACh

19
Q

Where does ACh bind?

A

Interphase between subunits (alpha gamma and alpha 8?)

20
Q

What efflux/influx occurs when the gate is open/

A

Na+ influx
K+ Efflux
This causes the intercellular region to become less negative - end plate potential

21
Q

What makes the end plate potential?

A

ACh binding to nicotinic receptors

22
Q

Does each vesicle have the same amount of ACh molecules in it and what is it called?

A

yes this is known as the quantum

23
Q

What happens when multiple vesicles release their quantum?

A

It has a combined affect on the voltage, causing a large depolarization building up - known as the end plate potential

24
Q

How does the end plate potential produce contraction?

A

The end plate potential reaches a threshold potential, leading to the opening of voltage activated sodium channels, which triggers a muscle action potenitial

25
Q

Which is graded, end plate potential or action potential?

A

End plate potential

26
Q

What can reduce the amplitude of the EPP?

A

Drugs

Toxins

27
Q

What happens when an end plate potential doesn’t reach the threshold?

A

No contraction occurs
Fibre spreads out
Loses size
Fades away to nothing

28
Q

What are the symptoms of neuromyotonia?

A

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

29
Q

What is the cause of neuromyotonia?

A

Mostly autoimmune - antibodies against voltage-activated K+ channels in the motor neurone resulting in hyperexcitability (repeated fitting)

30
Q

What are the drug treatments for neuromyotonia?

A

Anti-convulsants
carbamazepine
Phenytoin

31
Q

What are the characteristics of Lamber eaton myasthenic syndrome?

A

Muscle weakness in the limbs

?Small cell carcinoma of the lung

32
Q

What is the cause of LEMS?

A

Autoimmune - antibodies against voltage activated Calcium channels in the motor neurone terminal result in reduced cancium centry

33
Q

What is the drug treatment for LEMS?

A

Antcholinesterases and potassium channel blockers

34
Q

What are the characteristics of Myasthenia gravis?

A

Progressivley increasing muscle weakness during periods of activity
Presents with weakness of the eye and eyelid

35
Q

What is the cause of Myaesthenia gravis?

A

Autoimmune - antibodies against nicotinic ACh receptors in the endplate result in reduction in the number of functional channels and hence the amplitude of the end plate potential

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