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14.4: Voltage-gated Ion Channels

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Cell Biology

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Voltage-gated Ion Channels

14.4: Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.

Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of voltage-gated channels because these proteins show selective ion permeability based on ions' size and charge. For example, sodium ions, cannot pass through a potassium channel and vice versa.

Usually, these channels have an open and closed ion-conducting state. The ball and chain mechanism of action regulates the opening and closing of some classes of voltage-gated ion channels in response to the membrane potential. Here, in addition to the open and closed states, there is an inactivated state. As seen in the voltage-gated sodium channels, the inactivation gate acts as a plug or a lid that blocks the flow of sodium ions, which is the non-conducting state of the channel. Inherited or acquired defects in the sodium channel can cause abnormal neuronal firing seen in epileptic seizures, cardiac dysfunction, skeletal muscle weakness, and stiffness.

These channels have a vital role in various bodily functions. The voltage-gated calcium channels are pivotal in muscle contraction and neurotransmitter release. Potassium channels help repolarize the cell membrane after an action potential. Voltage-gated sodium channels help in membrane depolarization and propagation of the action potential.

A venomous snake, the Black mamba produces a deadly venom that blocks the voltage-gated potassium channels. This prevents the potassium ions from exiting the neuron during action potential propagation. Hence, the persistent depolarization by the sodium channels and prolonged release of the neurotransmitter acetylcholine may cause muscle hyperexcitability and convulsions.

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