L2b - Electrophysiology (2) Flashcards

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1
Q

Describe the path that action potentials take through the parasympathetic autonomic nervous system.

A

1) Central Nervous System (CNS)
2) Preganglionic Neurone
3) Synapse
4) Acetylcholine binds to Nicotinic Acetylcholine Receptor
5) Ganglionic Cell
6) Postganglionic Neurone
7) Acetylcholine binds to Muscarinic Acetylcholine Receptor
8) Target Organ

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2
Q

Describe the 2 different paths that action potentials can take through the sympathetic autonomic nervous system.

A

1) Central Nervous System (CNS)
2) Preganglionic Neurone
3) Sympathetic Ganglion
4) Acetylcholine binds to Nicotinic Acetylcholine Receptor
5) Synapse
6) Postganglionic Neurone
7) Norepinephrine binds to Alpha Norepinephrine Receptor Subtype
8) Norepinephrine binds to Beta Norepinephrine Receptor Subtype
8) Target Organ

1) Central Nervous System (CNS)
2) Preganglionic Neurone
3) Adrenal Gland
4) Acetylcholine binds to Nicotinic Acetylcholine Receptor
5) Synapse
6) Postganglionic Neurone
7) Norepinephrine binds to Alpha Norepinephrine Receptor Subtype
8) Epinephrine binds to Beta Norepinephrine Receptor Subtype

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3
Q

Describe epinephrine.

A
  • Commonly known as adrenaline

- Secreted from the adrenal medulla

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4
Q

Describe norepinephrine.

A
  • Released into blood as a stress hormone / neurotransmitter
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5
Q

Describe the pathway of action potentials through a neuromuscular junction.

A

1) Action potential arrives at axon terminal (depolarisation occurs as pre-synaptic membrane becomes more positive)
2) Voltage gated Ca2+ channels open
3) Ca2+ enters the cell
4) Ca2+ signals to vesicles
5) Vesicles move to the membrane
6) Docked vesicles release neurotransmitter by exocytosis
7) Neurotransmitter diffuses across the synaptic cleft and binds to nicotinic receptors

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6
Q

Describe Vx Gas.

A
  • Extremely toxic nerve agent
  • Cholinesterase inhibitor (breaks down acetylcholine)
  • ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase
  • Postsynaptic membrane ion channel closed; ions cannot pass
  • Glands and muscles are constantly being stimulated
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7
Q

State the symptoms of a low/moderate dose of Vx Gas.

A
  • Abnormally low / high blood pressure
  • Blurred vision
  • Chest tightness
  • Confusion
  • Cough
  • Diarrhoea
  • Drooling
  • Drowsiness
  • Excessive sweating
  • Eye pain
  • Headache
  • Increased urination
  • Nausea, vomiting and / or abdominal pain
  • Rapid breathing
  • Runny nose
  • Slow / fast heart rate
  • Small, pinpoint pupils
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8
Q

State the symptoms of a large dose of Vx Gas.

A
  • Convulsions
  • Loss of consciousness
  • Paralysis
  • Respiratory failure (possibly leading to death)
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9
Q

What are convulsions?

A

When body muscles contract and relax rapidly and repeatedly = uncontrolled actions

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10
Q

What leads to summative contraction (tetanic contraction) in skeletal muscle?

A

Repeated, high frequency action potentials

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11
Q

What does a repeated stimulus at the neuromuscular junction cause?

A

Greater number / frequency of skeletal muscle action potentials

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12
Q

What happens when action potentials summate?

A
  • Lead to a larger contraction
  • Overexcitation of Nicotinic Receptors
  • More action potentials in a short space of time causes larger contractions = tetanus
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13
Q

What does overexcitation of Nicotinic Receptors cause?

A
  • Sodium ion (Na+) build up
  • Tetanus
  • Involuntary contractions
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14
Q

State the 4 different states in which tension developed in a muscle fibre.

A

1) Twitch
2) Wave summation
3) Unfused (incomplete) tetanus
4) Fused (complete) tetanus

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15
Q

Sodium channels must first do what before another action potential is fired?

A

Must first recover from inactivation

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16
Q

What leads to muscle contraction?

A

A single action potential leads to the release of calcium from the sarcoplasmic reticulum, which leads to contraction

17
Q

Describe the all or nothing principle.

A
  • If stimulus is too small = few sodium channels will open = not enough to cause an influx of Na+ ions = NOTHING (no action potential sent)
  • If stimulus is of sufficient size / threshold reached = Na+ ions influx = depolarisation of neurone = ALL (action potential sent)
  • If stimulus is of large size / threshold surpassed = Na+ ions influx = depolarisation of neurone = ALL (action potential sent)

No difference caused by size of depolarisation

18
Q

Describe how voltage-gated ion channels inactivate.

A
  • Ball and chain mechanism

- Protein at the end of n-terminus = ‘ball’

19
Q

Describe how the recovery from inactivation can be measured.

A

By applying another square pulse:

  • A few milliseconds after the first one = little increase in current, few channels recovered
  • A significant period after the first one = gradual increase in current, most channels recovered
20
Q

Describe the properties of the Absolute Refractory Period.

A
  • Too few Na+ channels have recovered from inactivation

- Not possible to elicit an action potential (irrespective of how large stimulus is)

21
Q

Describe the properties of the Relative Refractory Period.

A
  • A proportion of Na+ channels have recovered

- Possible to elicit an action potential with greater stimulus

22
Q

Define ‘Refractory Period’.

A

Time period during which another action potential cannot be elicited.

23
Q

Why can’t tetanic contraction occur in cardiac muscle?

A

Because sodium channels take longer to recover from inactivation (refractory period is longer)

24
Q

Describe cardiac action potentials.

A
  • Cardiac action potentials do not elicit a summative contraction
  • Each action potential leads to a single contraction
  • They are no longer in duration
  • Cannot cause tetanus because the refractory period is too long

(Time scale is a lot longer)

25
Q

Describe Myasthenia Gravis.

A
  • Immune system mistakenly makes antibodies that attack the ACh receptor sites at the neuromuscular junction
  • Weakness in muscles improves with rest, because ACh stores get built up again
  • Edrophonium chloride (acetylcholinesterase inhibitor) improves condition because it prevents the breakdown of ACh, which allows for continued stimulation
26
Q

Describe Tetrodotoxin Poisoning.

A
  • Powerful neurotoxin
  • Blocks sodium conductance (Na+ channel blocker)
  • Blocks neuronal transmission in skeletal muscle
  • Inhibits firing of action potentials in neurones by binding to the voltage-gated sodium channels in the nerve cell membranes, and blocking the passage of Na+ into the neurone