Pathophysiology of tardive dyskinesia.
Animal models of persisting tardive dyskinesia have been developed in two species (rats and monkeys). Dyskinetic animals chronically treated with neuroleptics had significant decreases in glutamic acid decarboxylase and GABA in the substantia nigra, the medial globus pallidus, and the subthalamic nucleus, whereas animals without dyskinesias which had been treated similarly had a normal distribution of these biochemical parameters. These changes remained 2 months after neuroleptics were discontinued, and at that point there was a reduced turnover of striatal dopamine in the dyskinetic monkeys. These findings suggest that reduced GABA function in the substantia nigra may play a role in tardive dyskinesia.
D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002428:Cebus; D003342:Corpus Striatum / Q000503:physiopathology; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006801:Humans; D009434:Neural Pathways / Q000503:physiopathology; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology; D013378:Substantia Nigra / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase