Ion channels of the glycine receptors (GlyR) provide an inhibitory drive in the nervous system of vertebrates. Four agonist-binding <$E alpha> subunits and one <$E beta> subunit were cloned from the CNS of mammals (human, rat, and mouse), a bird (chicken), and a fish (zebrafish). Subunit composition determines pharmacological properties of the GlyR and function of the glycinergic synapses during development. Dysfunction of these receptors results in motor disorders (hyperekplexia, spasticity, and/or oscillatory phenomena), and mutations in the gene encoding the <$E alpha> subunit of GlyR underlie the molecular basis of these heritable diseases. Extra- and intracellular pharmacological tools can modulate the activity of GlyR channels. A recently discovered phenomenon of Ca-induced modulation of the GlyR suggests an important way of modulation of the activity of glycinergic synapses.

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