Tardive dyskinesia, dopamine receptors, and neuroleptic damage to cell membranes.
The long-term treatment of schizophrenic patients with neuroleptics is associated with neuroleptic accumulation in neuromelanin-containing cells with ensuing nigral cell damage. Thus, in addition to early or short-term up-regulation of D2 dopamine receptors, the late stage denervation supersensitivity may result in a further proliferation of D2 dopamine receptors in those parts of the human striatum controlling mouth-lips-tongue motion. Young individuals, upon reduction or removal of the neuroleptic, may have neural sprouting with subsequent D2 down-regulation and reversal of their dyskinesia. Older individuals may not readily exhibit sprouting and D2 down-regulation, possibly accounting for a more persistent form of dyskinesia.
Seeman
P
P
Department of Pharmacology, University of Toronto, Ontario, Canada.
D000818:Animals; D014150:Antipsychotic Agents / Q000009:adverse effects*; D002462:Cell Membrane / Q000187:drug effects*; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D006801:Humans; D011954:Receptors, Dopamine / Q000502:physiology*
D014150:Antipsychotic Agents; D011954:Receptors, Dopamine