NICOTINE POTENTIATION OF HALOPERIDOL-INDUCED CATALEPSY - STRIATAL MECHANISMS

Nicotine potentiated the catalepsy produced by haloperidol. The excito toxin quinolinic acid (QA) selectively destroys striatal neurons when injected directly into the striatum. Bilateral QA lesions of the rat s triatum (150 nmol) significantly reduced the catalepsy produced by hal operidol as well as the ability of nicotine to potentiate haloperidol- induced catalepsy. A second experiment examined whether the ability of nicotine to potentiate haloperidol-induced catalepsy was associated w ith a potentiation of dopamine turnover following haloperidol. Nicotin e alone produced a mild increase in dopamine turnover relative to sali ne treated controls while haloperidol produced a marked increase in do pamine turnover relative to saline- and nicotine-treated controls. How ever, the combined administration of haloperidol and nicotine did not further elevate dopamine turnover over that observed following haloper idol alone. The results indicated that 1) nicotine could not potentiat e haloperidol-induced catalepsy without an intact striatum and 2) the behavioral effect of nicotine and haloperidol cotreatment was not due to any change in dopamine turnover.