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Regulation The ion channel is regulated by a neurotransmitter ligand and is usually very selective to one or more ions like Na+, K+, Ca2+, or Cl-. Such receptors located at synapses convert the chemical signal of presynaptically released neurotransmitter directly and very quickly into a postsynaptic electrical signal. This is in contrast to the more slowly signaling metabotropic receptors which are not themselves ion channels but rather may be linked to them through complex intracellular second messenger cascades (e.g. G protein-coupled receptors). Many LGICs are additionally modulated by allosteric ligands, by channel blockers, ions, or the membrane potential. Example: nicotinic acetylcholine receptor The prototypic ligand-gated ion channel is the nicotinic acetylcholine receptor. It consists of a pentamer of protein subunits, with two binding sites for acetylcholine, which, when bound, alter the receptor's configuration and cause an internal pore to open. This pore, permeable to Na+, allows Na+ ions to flow down their electrochemical gradient into the cell. With a sufficient number of channels opening at once, the intracellular Na+ concentration rises to the point at which the positive charge within the cell is enough to depolarize the membrane, and an action potential is initiated. Classification and examples Many important ion channels are ligand-gated, and they show a great degree of homology at the genetic level. The Ligand-gated ion channels are classified into four superfamilies: Clinical relevance Ligand-gated ion channels are likely to be the major site at which anaesthetic agents have their effects, although unequivocal evidence of this is yet to be established. In particular, the GABA and NMDA receptors are affected by anaesthetic agents at concentrations similar to those used in clinical anaesthesia. Also Known As: Chemically Gated Ion Channels. See also | ||||||||||
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