Nerve & Muscle Flashcards

1
Q

Describe how a resting potential is maintained

A

K+ moves out of the cell via the K+ channels
Na+ moves into cell via Na+ channels
Na+/K+ ATPase actively pumps 3Na+ out of the cell and 2K+ into the cell to maintain concentration gradient
Final resting potential is approx -70mv

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2
Q

Describe how an action potential is generated

A
  1. Membrane is depolarised so its membrane
  2. Voltage gated Na+ channels allow Na+ into the cell
  3. Voltage gated Na+ channels start to inactivate
  4. Voltage gated K+ channels open allowing K+ to leave the cell causing repolarisation
  5. K+ and Na+ channels closed
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3
Q

What’s the difference between chemical and electrical synapses?

A

Electrical synapses have a direct passage of current between neurones
Chemical synapses have to release vesicles containing neurotransmitter to affect the target cell

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4
Q

What are the features of an electrical synapse?

A
  • more rapid
  • can be bidirectional
  • enable the synchronised activity of groups of cells
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5
Q

What are gap junctions?

A

Channels called connexons in the pre and post synaptic membrane join to form complexes creating electrical continuity between the two cells

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6
Q

What are the features of a chemical synapse?

A

Unidirectional
Slower than electrical

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7
Q

In a chemical synapse, how are neurotransmitters cleared from the synapse?

A

Enzymatic degradation
Reuptake by specific transporters
Diffuse out of the synapse

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8
Q

What are the two types of post synaptic receptors?

A

Ionotropic
Metabotropic

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9
Q

What type of post synaptic receptor is this?..
- open/close in response to the binding of the neurotransmitter
- fast acting

A

Ionotropic

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10
Q

What type of post synaptic receptor is this?
- requires G proteins (secondary messangers)
- slow and more persistent response

A

metabotropic

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11
Q

What is a neuromodulator?

A

It alters the strength of transmission between neurons by affecting the amount of neurotransmitter produced and released

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12
Q

What is the function and drug effect/pathology of acetyl choline?

A

Main parasympathetic neurotransmitter, involved in NMJ, learning and memory
Botox causes paralysis by blocking ACh release

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13
Q

What is the function and drug effect/pathology of noradrenaline?

A

Used by the sympathetic nervous system, alertness, mood
Beta adrenergic receptor blockers used to treat cardiovascular pathologies e.g. hypertension and heart faliure

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14
Q

What is the function and drug effect/pathology of GABA?

A

Main inhibitory neurotransmitter
Anti-anxiety drugs bind to GABA receptors suppressing overactive brain areas linked to worry

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15
Q

What is the function and drug effect/pathology of Glutamate?

A

Main excitatory neurotransmitter, learning, memory
High levels are associated with schizophrenia

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16
Q

What is the function and drug effect/pathology of serotonin?

A

Influences sleep, appetite, learning/memory and mood
Selective uptake inhibitors are used to treat depression

17
Q

What is the function and drug effect/pathology of dopamine?

A

Pleasure neurotransmitter, influences learning/memory, motivation/behaviour, mood and movement
Drugs that increase dopamine are used in treating Parkinson’s

18
Q

What does a single motor unit consist of?

A

A single motor neurone and all the skeletal muscle fibres innervated by that neurone

19
Q

How is fine precision in the muscle enabled?

A

Smaller muscles having few muscle fibres in each motor unit

20
Q

What are the features of a neuromuscular junction?

A

Chemical synapse
1:1 transmission
unidirectional
Inherent time delay (0.5-1ms)
Site for many diseases and action of many pharmacological drugs

21
Q

Label this diagram
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A

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22
Q

Describe how acetylcholine is removed from the synapse

A

After ACh has bound to the receptor on the post synaptic cell it is hydrolysed by acetylcholinesterase
Choline is recycled back into the presynaptic terminals to make more ACh
Acetate quickly diffuses into the surrounding medium

23
Q

Describe the structure of the nicotinic acetylcholine receptor

A

ACh gated Na+ channels
Made of 5 polypeptide subunits
(Two alpha, one each of beta, sigma and gamma)
2 ACh molecules are needed to stimulate the receptor

24
Q

What does succinylcholine do and how is it used clinically?

A

Causes muscle paralysis by affecting ACh receptors
Used during surgery to relax skeletal muscle
Patient is requires to be artificially ventilated

25
Q

What does succinylcholine do and how is it used clinically?

A

Causes muscle paralysis by affecting ACh receptors
Used during surgery to relax skeletal muscle
Patient is requires to be artificially ventilated

26
Q

How does the toxin produced by clostridium botulinum affect the NMJ?

A

It prevents exocytosis of ACh from the synaptic vesicles
Therefore muscle does not contract

27
Q

How can Botox be used clinically?

A

Can be used to relax muscles to help with strabismus (cross eyes), biepharospasm (eyelid spasms) or cerebral palsy

28
Q

What are the symptoms of myasthenia gravis?

A

Muscle weakness that increases during periods of activity and improves after rest
Eye related issues
- Ptosis (drooping of upper eyelid)
- Diplopia (double vision)
Face and throat related issues
- Altered speech
- Dysphagia (difficulty swallowing)
- Loss of facial expression

29
Q

What is myasthenia gravis?

A

Autoimmune condition
Caused by antibodies that competitively inhibit the nAChR on the motor end plate
NMJ less responsive to ACh - muscle weakness

30
Q

What is the treatment for myasthenia gravis?

A

Long term acting anti-cholinesterases (neostigmine)
Prevent breakdown of ACh - more ACh available in the synapse to compete with the antibodies for the nAChR

31
Q

What is Lambert-Eaton myasthenic syndrome?

A

Autoimmune disease
Antibodies formed against the voltage gated Ca2+ channels on the presynaptic nerve terminal at NMJ
Prevents ACh release
Condition is also associated with small cell lung cancer

32
Q

What are the symptoms of Lambert Eaton myasthenic syndrome?

A

Weakness in muscle limbs, fatigue, autonomic dysfunction (e.g. blurred vision, dry mouth)
Symptoms almost always precede detection of cancer

33
Q

What is the treatment for Lamert-Eaton myasthenic syndrome?

A

Using immunosuppressants
Use a K+ channel blocker - blocks K+ channels on presynaptic nerve terminal
This delays the repolarisation of the membrane so prolongs depolarisation of the presynaptic membrane
This enhances Ca2+ entry into the terminal so facilitates release of ACh improving neuromuscular transmission

34
Q

What is the difference between the autonomic and somatic nervous system?

A

Autonomic - involuntary responses
Somatic - voluntary responses

35
Q

What is the difference between the sympathetic and parasympathetic nervous system?

A

The sympathetic does fight/flight responses such as increased heart rate or dilated pupils
Parasympathetic does the opposite so relaxes e.g decreased heart rate or constricted pupils

36
Q

Describe the structure of a multipolar neurone

A

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37
Q

Describe the structure of a unipolar neurone

A

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