Comparative neuropharmacology of antianxiety drugs.
Over the past five years, the mechanisms of action of several classes of antianxiety drugs have been clarified. Benzodiazepines, triazolopyridazines, and barbiturates seem to produce their anxiolytic effects by interacting with a specific high affinity receptor (viz. benzodiazepine receptor) in the brain. The benzodiazepine receptor is functionally and perhaps structurally coupled to a receptor for the major inhibitory neurotransmitter GABA as well as a chloride channel or ionophore. Taken together, this receptor "complex" may mediate the behavioral effects of a number of chemically diverse antianxiety agents. Evidence for the role of the benzodiazepine-GABA receptor-chloride ionophore complex inthe mechanism of action of minor tranquilizers and a possible interaction with the novel anxiolytic buspirone is discussed.
D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology*; D001569:Benzodiazepines / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D006801:Humans; D011956:Receptors, Cell Surface / Q000378:metabolism; D011963:Receptors, GABA-A; D013329:Structure-Activity Relationship; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D014151:Anti-Anxiety Agents; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D001569:Benzodiazepines; D005680:gamma-Aminobutyric Acid; D002118:Calcium