Characterization of the role of serotonin in the regulation of phencyclidine's behavioral and electrophysiological effects

Abstract

Electrophysiological and behavioral methods were utilized in conjunction with either specific brain lesions or drug administration to evaluate serotonin's modulatory influence on phencyclidine's actions. Dorsal raphe (DR) and medial raphe (MR) nucleus lesions were preformed to destroy serotonin cell bodies, while ritanserin and parachloroamphetamine (PCA) were used to remove or inhibit serotonin. The DR lesions changed phencyclidine's electrophysiological response in only the VTA (A10), while the MR lesions effected only the SN (A9) neurons. Thus the DR innervates the VTA, and the MR innervates the SN. The PCA, ritanserin, and DR groups showed a potentiated locomotor response to phencyclidine with no change in the animals spontaneous activity. The MR group showed an increase in spontaneous activity, but when normalized for this, there was no potentiation of the phencyclidine effect. Thus, the drug potentiation of the locomotor hyperactivity appears to be mediated through the DR serotoninergic system and A10 dopamine system.