voltage gated K channels Flashcards

1
Q

What is the general function of potassium (K⁺) channels?

A

regulate membrane potential, repolarization

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2
Q

What are maxi-K channels (BK channels)?

A

large-conductance calcium-activated K⁺ channels that respond to both membrane voltage and intracellular calcium levels.

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3
Q

What are the main structural components of maxi-K channels?

A

a subunit and B subunit
calcium binding domains

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4
Q

What is the role of the α subunit in maxi-K channels

A

ion-conducting pore and contains both a voltage-sensor domain and intracellular calcium-binding sites that control the opening of the channel.

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5
Q

What is the role of the B subunit in maxi-K channels

A

enhance the channel’s calcium sensitivity, influence the channel’s voltage dependence, and regulate the kinetics of gating.

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6
Q

How does intracellular calcium influence maxi-K channel gating?

A

binds to the calcium-binding sites in the C-terminal of the α subunit, increasing the probability of channel opening even at lower voltages.

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7
Q

What physiological processes are maxi-K channels involved in?

A

neuronal firing, smooth muscle contraction, vascular tone, and neurotransmitter release by controlling membrane repolarization

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8
Q

How does the β1 subunit affect maxi-K channels in smooth muscle?

A

increases calcium sensitivity

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9
Q

What effect does β4 subunit expression have on neuronal maxi-K channels?

A

regulates excitability

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10
Q

What are the consequences of mutations in maxi-K channels?

A

hypertension, epilepsy, and cerebellar ataxia

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11
Q

What are TREK channels and how are they activated?

A

part of the two-pore domain K⁺ (K2P) family. They are mechanosensitive and activated by membrane stretch, changes in temperature, pH, and certain lipids.

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12
Q

What physiological role do TREK channels play?

A

regulate neuronal excitability, pain sensation by maintaining resting membrane potential

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13
Q

How do TREK channels contribute to neuroprotection?

A

protect neurons during conditions like ischemia and hypoxia by hyperpolarizing the membrane, reducing neuronal excitability

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14
Q

What are KATP channels and how are they regulated?

A

ATP-sensitive K⁺ channels They close when intracellular ATP levels are high and open when ATP is low, allowing K⁺ efflux to stabilize membrane potential.

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15
Q

What is the physiological role of KATP channels in the pancreas?

A

In pancreatic β-cells, KATP channels regulate insulin secretion. When ATP levels are high after glucose metabolism, KATP channels close, leading to cell depolarization and insulin release.

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16
Q

What are the clinical implications of KATP channel dysfunction?

A

neonatal diabetes, hyperinsulinism, and cardiomyopathies

17
Q

What is the rationale for using KATP channel inhibitors in the treatment of type 2 diabetes?

A

used to stimulate insulin secretion from pancreatic β-cells.
KATP inhibitors close these channels directly, bypassing ATP-mediated regulation, resulting in increased insulin secretion to help control blood glucose levels.

18
Q

What is the function of calcium-activated K⁺ channels (KCa) during the action potential?

A

contribute to afterhyperpolarization by allowing K⁺ outflow in response to increased intracellular calcium, which prolongs the refractory period.

19
Q

How do inward rectifier K⁺ channels (Kir) stabilize the action potential?

A

help stabilize the resting membrane potential and facilitate slow repolarization after action potentials, contributing to the overall excitability of the neuron

20
Q
A