Differential effects of acute and chronic administration of haloperidol on homovanillic acid levels in discrete dopaminergic areas of rat brain.
After acute administration of haloperidol, homovanillic acid (HVA) levels were increased in the prefrontal cortex, anterior cingulate cortex, discrete limbic areas and A14 dopamine (DA) neurons. The maximal effect of haloperidol was attained more slowly in the prefrontal cortex and amygdala than in the other regions. The ED50 of haloperidol was 0.03 mg/kg in the prefrontal cortex, but was 0.06-0.07 mg/kg in other areas examined. After repeated administration of haloperidol, tolerance to the HVA increase was observed in the striatum and all limbic areas examined, the amygdala being the most susceptible to this tolerance. In contrast, no tolerance was found in the anteromedial and suprarhinal DA neurons of the prefrontal cortex and A14 DA neurons. These results suggest that the prefrontal cortex may be a possible site for the antipsychotic action of haloperidol. On the other hand, no change of HVA levels in the A12 and A13 DA neurons of the hypothalamus was observed after haloperidol treatments, suggesting a lack of neuronal feedback mechanism in the A12 and A13 DA neurons.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology*; D006719:Homovanillic Acid / Q000378:metabolism*; D008297:Male; D010648:Phenylacetates / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D010648:Phenylacetates; D006220:Haloperidol; D004298:Dopamine; D006719:Homovanillic Acid