EFFECTS OF BILATERAL LESIONS IN THE STRIATUM OR NUCLEUS ACCUMBENS ON THE CATALEPTOGENIC ACTIVITY OF NEUROLEPTICS IN RATS

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Abstract
To investigate the role of the striatum and nucleus accumbens in neuroleptic-induced catalepsy, bilateral electrocoagulations were made or microinjections of 6-hydroxydopamine (6-OHDA) were given to rats in these brain regions, and the cataleptogenic activity of neuroleptics was measured. Electrocoagulation in these regions caused a highly specific destruction of brain tissue, and 6-OHDA decreased the levels of dopamine in the injected region with little effect on these levels in other regions. The cataleptogenic activity of haloperidol was enhanced by the electrocoagulation in the striatum at 2 days after the operation, but was weakened from 7 days on. The electrocoagulation weakened the catalepsy induced by chlorpromazine, thioridazine and ID-4708 [1-[3-(2-amino-4-fluorobenzoyl)-propyl]-4-hydroxy-4-(3-trifluoromethylphenyl) piperidine] (a new butyrophenone derivative), but enhanced that by clozapine at 2 wk after the operation. Microinjection of 6-OHDA into the striatum enhanced the catalepsy induced by the 5 neuroleptics used. The lesions in the nucleus accumbens had fewer effects on catalepsy than did those in the striatum. The striatum more than the nucleus accumbens is involved in producing catalepsy with neuroleptics, and the enhancement of catalepsy by electrocoagulation in the striatum is characteristic of clozapine.