Neurobiology Flashcards

1
Q

What happens if the APs causes K+ to increase in Normal Muscle?

A

Increased [K+] exerts depolarizing effect on membrane potential –> High permeability to Cl-, so Cl- moves into cell to resist depolarization.

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2
Q

What happens if the APs causes K+ to increase in Myotonic Muscle?

A

Increased [K+] exerts depolarizing effect on membrane potential –> In myotonia congenita the depolarization sustained discharge of action potentials.

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3
Q

What does Resting Potential reflect?

A

Resting membrane potentials reflect the weighted average of equilibrium potentials of the ions that can across the membrane.

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4
Q

True or False: Is action potential threshold typically close to the resting potential.

A

True.

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5
Q

Conditions that after resting potential often cause aberrant neural signaling.

A
  • Alteration of equilibrium potential (alterations in extracellular K+)
  • Altered channel activity.
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6
Q

What happens to [K+] in Hyperkalemia?

A

elevated extracellular k+

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7
Q

What is the concentration of [K+] in normal conditions?

A
  • Resting potential dominated by k+

- Low extracellular K+

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8
Q

Where the neurotransmitters are stored?

A

In vesicles

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9
Q

What is the sequence of events in transmission from nerve to muscle?

A
  1. Action potential depolarizes nerve terminal, leading to the opening of Ca2+channels and Ca2+entry
  2. Resulting increase in intracellular Ca2+concentration causes ACh filled vesicles to fuse with nerve terminal membrane Released ACh diffuses across the synaptic cleft, binds to and activates postsynaptic ACh receptors. Activation of ACh receptors produces a non-selective cation current, which is mostly an inward movement of Na+at normal membrane voltages
  3. Inward movement of Na+depolarizes muscle fiber, leading to action potential
  4. Released ACh is degraded by acetylcholinesterase
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10
Q

What is the function of the Botulinum toxins?

A

Botulinum toxin disrupts proteins involved in ACh release and hence renders the nerve unable or less able to elicit contraction in the muscle.

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11
Q

Important properties of synaptic transmission at NMJ

A
  • Transmitter (ACh) stored in vesicles.
  • Depolarization –> calcium influx –> release
  • ACh activates receptor/Channel complexes
  • ACh removed by enzymatic degradation
  • Presynaptic AP –> muscle AP (one to one)
  • One directional
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