Abstract
Benzodiazepines exert their effects by facilitating neurotransmission in GABAergic synapses, probably by increasing the affinity of the GABA receptor to GABA. Stimulation of GABA receptors (at least of the A type) opens chloride ion channels which inhibits the ability of the cell (e.g. monoaminergic or cholinergic) to conduct nerve impulses. The endogenous ligand for the benzodiazepine receptor is probably a peptide, which is able to induce "anxiety" in rats. Thus, if the benzodiazepines are receptor agonists, the endogenous ligand would be an antagonist. The clinical effects resulting from the above mechanism of action (anticonvulsant, muscle relaxant, anxiolytic, sedative-hypnotic and amnesic) are discussed with special attention to preoperative sedation in dental practice.
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