Wang Z, Rebec G V
Department of Psychology, Indiana University, Bloomington 47405, USA.
Brain Res. 1996 Mar 4;711(1-2):64-72. doi: 10.1016/0006-8993(95)01401-2.
Single-unit activity was recorded from the amygdaloid complex in freely moving rats during an infusion of amphetamine directly into the recording site. Relative to the quiet resting period prior to the infusion, amphetamine routinely increased neuronal activity within 5-15 min after infusion onset, and this response continued for at least another 30 min. It was generally accompanied by marked increases in sniffing, rearing, locomotion, and grooming as well as by a tendency to turn to the ipsilateral side. Haloperidol and clozapine, typical and atypical antipsychotic drugs, respectively, were then tested in their ability to reverse these neuronal and behavioral effects. Both antipsychotics were administered subcutaneously at behaviorally effective doses within 10 min after termination of the amphetamine infusion. Haloperidol (1.0 mg/kg) failed to reverse the amphetamine-induced increase in amygdaloid neuronal activity and required more than 20 min to exert a partial blockade of the accompanying behavioral activation. Clozapine (10.0 mg/kg), in contrast, blocked the excitatory effects of amphetamine on all tested neurons and also blocked most amphetamine-induced behaviors within 10 min. Taken together, these results, which support other lines of electrophysiological evidence, point to the amygdala as a critical site in the differential behavioral effects of typical and atypical antipsychotic drugs.
