Haloperidol-induced catalepsy is mediated by postsynaptic dopamine receptors.
Antipsychotic or neuroleptic drugs, which block central dopamine receptors, produce a behavioural state in animals in which they fail to correct externally imposed postures. This is referred to as catalepsy. Previous lesion studies have shown that the dopamine receptors in the striatum are involved in this neuroleptic-induced catalepsy. Dopamine receptors, identified by the specific, high-affinity binding of the potent neuroleptic haloperiodol, have been shown to be equally distributed postsynaptically on striatal neurones and presynaptically on cortico-striatal terminals. Because the electrolytic lesioning studies have unavoidably damaged both pre- and postsynaptic striatal dopamine receptors, it is not known whether these two receptors are separately involved in neuroleptic-induced catalepsy. Using kainic acid and cortical ablation to destroy postsynaptic and presynaptic dopamine receptors, respectively, the present study demonstrates that the cataleptic effects of haloperidol are apparently mediated by dopamine receptors localised postsynaptically on striatal neurones.
D000818:Animals; D002375:Catalepsy / Q000139:chemically induced*; D002540:Cerebral Cortex / Q000502:physiology; D003342:Corpus Striatum / Q000187:drug effects; D006220:Haloperidol / Q000494:pharmacology*; D006801:Humans; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects*; D013570:Synaptic Membranes / Q000187:drug effects / Q000648:ultrastructure
D011954:Receptors, Dopamine; D006220:Haloperidol; D007608:Kainic Acid