Acute thioridazine stimulates mesolimbic but not nigrostriatal dopamine release: demonstration by in vivo electrochemistry.
In vivo electrochemical techniques were employed to demonstrate that haloperidol and (+)-butaclamol increased the release of dopamine (DA) in the striatum and nucleus accumbens, whereas thioridazine stimulated DA release only in the accumbens. The stimulatory effect of thioridazine was reversed by gamma-butyrolactone. Given that gamma-butyrolactone inhibits DA neuronal activity, these data indicate that the regional selectivity of thioridazine on DA release is due to its ability to preferentially stimulate DA cell firing in the ventral tegmental (A10) area and suggest that its antipsychotic properties depend on its actions in the mesolimbic DA system.
D015107:4-Butyrolactone / Q000502:physiology; D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology; D002069:Butaclamol / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D004563:Electrochemistry; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D009714:Nucleus Accumbens / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012686:Septal Nuclei / Q000187:drug effects*; D013881:Thioridazine / Q000494:pharmacology*
D014150:Antipsychotic Agents; D002069:Butaclamol; D006220:Haloperidol; D013881:Thioridazine; D015107:4-Butyrolactone; D004298:Dopamine