14.4:
Voltage-gated Ion Channels
Voltage-gated ion channels are a class of transmembrane proteins that open and close in response to changes in the membrane potential — the voltage difference across a membrane.
These channels have a voltage-sensor domain that moves under the influence of the charge and a highly selective gated transmembrane channel for the ions' movement.
On receiving an impulse, the cell membrane depolarizes, becoming more positive. This voltage difference shifts the voltage sensors upwards, opening the gated channel, which allows ions to move down their concentration gradient.
Depending on the ion-specificity, there are four types of voltage-gated ion channels.
Voltage-gated sodium channels, abundantly found in the neurons, aid in the rapid influx of sodium ions, causing membrane depolarization.
Voltage-gated potassium channels, found in diverse cell and tissue types, allow rapid efflux of potassium ions, restoring the membrane potential.
Voltage-gated calcium channels allow the influx of calcium ions that trigger neurotransmitters' release into the synapse.
Lastly, the voltage-gated chloride channels permit chloride ions' influx and help regulate the cell volume. These are distributed in neurons, muscles, and kidneys.
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.
Leitura Sugerida
- de Lera Ruiz, Manuel, and Richard L. Kraus. "Voltage-gated sodium channels: structure, function, pharmacology, and clinical indications." Journal of medicinal chemistry 58, no. 18 (2015): 7093-7118.
- Bachmann, Magdalena, Weiwei Li, Michael J. Edwards, Syed A. Ahmad, Sameer Patel, Ildiko Szabo, and Erich Gulbins. "Voltage-gated potassium channels as regulators of cell death." Frontiers in Cell and Developmental Biology (2020): 1571.