The effect of butaclamol and of other neuroleptic agents on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity.
The effects of the two enantiomers of butaclamol and of several neuroleptics on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity was investigated. The (+) but not the (-) enantiomer of butaclamol reverses the apomorphine-elicited enzyme inhibition. (+) Butaclamol is more potent than the other tested neuroleptics. All the tested neuroleptics reverse the apomorphine-elicited enzyme inhibition but their relative potency differs. Using two criteria, namely the concentrations of neuroleptics required to reverse enzyme inhibition maximally or by 25%, the order of decreasing potency is as follows: (+) butaclamol, fluphenazine, haloperidol, pimozide, chlorpromazine. The results suggest that the reversal of apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity is a valid test model for screening antipsychotic drugs.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D003342:Corpus Striatum / Q000648:ultrastructure; D003986:Dibenzocycloheptenes / Q000627:therapeutic use*; D004347:Drug Interactions; D066298:In Vitro Techniques; D007536:Isomerism; D008297:Male; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000201:enzymology*; D014149:Tranquilizing Agents / Q000627:therapeutic use*; D014446:Tyrosine 3-Monooxygenase / Q000037:antagonists & inhibitors*
D003986:Dibenzocycloheptenes; D014149:Tranquilizing Agents; D014446:Tyrosine 3-Monooxygenase; D001058:Apomorphine