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Benzodiazepines (BZDs) facilitate GABA-A action by increasing the frequency of chloride channel opening resulting in hyperpolarization of neurons and decreased firing, thus producing a calming effect on the brain by reducing excitatory neurons.
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GABA is an inhibitory neurotransmitter present in abundance in the cortex and limbic system. There are three types of GABA receptors; A, B, and C. However, BZDs only act on GABA-A receptors. Each receptor complex contains 2 GABA-binding sites and 1 BZD-binding site and is composed of five subunits two alpha, two betas, and one gamma. BZDs do not bind to the same receptor site on the receptor complex as the endogenous ligand GABA, but to distinct BZD-binding sites at the interface between the alpha and gamma subunits. Binding results in a conformational change in the chloride channel of the GABA-A receptor, which results in hyperpolarization of the cell and causes inhibitory effects of GABA throughout the central nervous system.
By increasing the frequency of chloride channel opening, resulting in hyperpolarization of neurons and decreased firing, benzodiazepines (BZDs) facilitate GABA-A action and exert a calming effect on the brain by reducing neuronal excitability.
Both the limbic and the cortex contain large amounts of GABA, an inhibitory neurotransmitter. GABA receptors come in three different subtypes: A, B, and C. BZDs only affect GABA-A receptors. They compose each receptor complex of five subunits: two alpha, two betas, and one gamma, and contain two GABA-binding sites and one BZD-binding site. BZDs bind to distinct BZD-binding sites at the interface between the alpha and gamma subunits rather than a single receptor site on the receptor complex as in the endogenous ligand GABA.