Effects of ethanol in a putative rodent model of tardive dyskinesia.

The effects of acute challenge with ethanol were studied in a putative rodent model of tardive dyskinesia. Chronic administration of fluphenazine elicited vacuous chewing movements (VCMs) in the rat. Neuroleptic-induced VCMs were dose dependently suppressed by ethanol in a behaviorally specific fashion. Suppression by ethanol of neuroleptic-induced VCMs was reversed by pretreatment with the benzodiazepine inverse agonist Ro 15-4513 (2.5 mg/kg). These findings suggest that ethanol may acutely suppress neuroleptic-induced dyskinesias in humans via stimulation of GABAA receptors and are compatible with the previously reported clinical effects of alcohol consumption on the extrapyramidal system. Treatment strategies focussed on GABAergic stimulation deserve further investigation in the management of tardive dyskinesia.