Ion channels are proteins that form pores and help in creating and controlling small voltage gradient across the plasma membrane. This is made possible through permitting the flow of ions through the electrochemical gradient. The ion channels are found at the membranes of biological cells and they are responsible for regulation of ions on the membranes of cells (Catterall, 1996). They are fundamental membrane proteins that form sub units in circular pattern that form around a pore filled with water from end to end the plane of the membrane.
Ion channels are cell membrane proteins that produce signals and respective changes and stimuli in the electrical potential of the Trans membrane. They transmit electrical signals to respond to extra cellular ligands, transmit membrane potential changes along the cell membrane plane for long distances, and respond to intracellular second messengers changes and also respond to regulatory proteins with ion conductance and membrane potential changes (Catterall, 1996).
When ion channels respond primarily to specific extracellular transitions they are named after them; for example ligand-gated ion channels respond primarily to extracellular ligands, others include the voltage-gated ion channels that respond to specific ions (Catterall, 1996). The gating refers to opening and closing of the channels depending on the plasma membrane voltage gradient. For the ligands the gating is controlled by the binding of the ligands on the channel.
Voltage gated ion channels such as voltage gated sodium channels; voltage gated calcium channels and voltage gated potassium channels generate propagated electrical signals in excitable cells such as neurons (Hille, 2001). They respond to Trans membrane potential changes that is produced through the binding of neural transmitters to ligands gated ion channels they then activate to produce action potential and propagate the changes in the membrane potential on the cell’s surface or through a nerve axon or a muscle filament (Hille, 2001).
The ion channel’s activation opens a specific Trans membrane pore that allow specific ions circulate down their electromagnetic gradient and thus move either in or out of the cell (Hille, 2001). Activation of sodium and calcium channels in most cases results to the ions moving inward and the cell depolarize. On the other hand potassium channel activation results to potassium ions moving outward and also cell re-polarization or cell hyper polarization.
In the event of action potential occurring small changes in the potential of the membrane activates the voltage gated sodium channels for a very short period of time (few milliseconds). The activation of voltage gated sodium channels produces a large depolarization which in turn activates the voltage gated calcium channels that allow the entry of calcium in to the cell and thus prolonging the action potential depolarization phase (Kass, 2006). The prolonged demoralization due to the sodium and calcium channels is put to an end through activating voltage gated and calcium activated potassium channels that act by cell re polarizing and cell hyper polarizing (Kass, 2006).
Potassium channels are also for the most part responsible in maintaining the quiescent of the cell membrane potential at negative values, and regulation of it in the intracellular second messengers’ action (Catterall, 1996). The activation of the voltage gated ion channels causes an increase in the permeability which is biphasic. Immediately after depolarization the sodium calcium or potassium permeability dramatically increases for a period of 0.5 to hundred milliseconds and consequently decreases for a period of 2 milliseconds to some few seconds to the baseline level (Catterall, 1996).
This is the biphasic action which can be accounted for in two experimentally separable gating processes responsible for controlling the rate and voltage dependence of the permeability increase following depolarization and inactivation which control the dependence of rate and voltage of the consequent come back of the ion permeability during a maintained depolarization to the resting level.
Catterall, W.A. (1996). Introduction: Ion channels in plasma membrane signal transduction. Journal of Bioenergetics and Biomembranes. Vol.28, (3), p. 217-218
Hille, B. (2001). Ion channels of excitable membranes. Ed. 3, Sunderland, Mass: Sinauer Associates
Kass, R.S. (2006). Sodium Channel Inactivation in Heart: A Novel Role of the Carboxy-Terminal Domain. Journal of Cardiovascular Electrophysiology. Vol.17 (1), p. 21-25
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