Tardive dyskinesia: a role for the endogenous opioid system.
Neuroleptic-induced tardive dyskinesia represents a major serious side-effect of chronic therapy with neuroleptic drugs. The pathomechanisms underlying this disorder are not well understood. Although the dopaminergic supersensitivity theory has gained most attention, there is evidence to suggest involvement of other transmitter systems. In this paper I shall discuss the possibility that the endogenous opioid system may be involved in the pathophysiology of tardive dyskinesia.
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D000818:Animals; D014150:Antipsychotic Agents / Q000009:adverse effects* / Q000494:pharmacology; D003342:Corpus Striatum / Q000378:metabolism / Q000503:physiopathology; D004298:Dopamine / Q000502:physiology; D004409:Dyskinesia, Drug-Induced / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D004723:Endorphins / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D006801:Humans; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D011957:Receptors, Opioid / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D014150:Antipsychotic Agents; D004723:Endorphins; D011954:Receptors, Dopamine; D011963:Receptors, GABA-A; D011957:Receptors, Opioid; D005680:gamma-Aminobutyric Acid; D006220:Haloperidol; D004298:Dopamine; D009638:Norepinephrine