Abstract
Buspirone (BuSpar®), a clinically effective anxiolytic, has been found in clinical trials to produce effects which suggest antidepressant efficacy. As antidepressants down-regulate type 2 serotonin (5-HT2) receptors when given chronically to laboratory animals, we investigated whether buspirone would have similar effects; the possibility that chronic buspirone administration would affect β-adrenergic, D-2 dopaminergic, and γ-aminobutyric acid (GABA) receptor binding was also investigated. When chronically administered in a regimen which reflected activity in an animal model of anxiety, buspirone produced significant decreases in in vitro 5-HT2 and β-adrenergic receptor binding but was without effect on D-2 dopaminergic of GABAergic binding. Ligand saturation experiments revealed that the decrease in 5-HT2 binding was due to a decrease in the maximal concentration of binding sites. These data demonstrate that chronic administration of buspirone to animals produces effects which suggest the potential for antidepressant efficacy in clinical use.
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