title: GABA dysfunction in the pathophysiology of tardive dyskinesia.
abstract: Pharmacologic treatments which diminish central dopaminergic transmission improve symptoms of tardive dyskinesia (TD). These clinical data, supported by results from animal model studies, have provided a basis for the dopamine (DA) receptor hypersensitivity hypothesis of TD. Since its initial formulation, however, knowledge of the multiple effects of prolonged neuroleptic administration in mammalian CNS has greatly expanded. Clinical and animal model studies carried out independently now both suggest that GABA-mediated neuronal tracts of the basal ganglia are important, perhaps pivotal, in TD. Thus, we would extend the DA hypothesis of TD to include the idea that neuroleptic-induced DA receptor hypersensitivity in striatum results in GABA system hypofunction in striatal projection areas in those individuals who develop TD.
authors.forename: C A
authors.initials: CA
authors.lastname: Tamminga
authors.forename: G K
authors.initials: GK
authors.lastname: Thaker
authors.forename: T N
authors.initials: TN
authors.lastname: Chase
mesh_terms: D001921:Brain / Q000503:physiopathology; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D006801:Humans; D009434:Neural Pathways / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D011954:Receptors, Dopamine / Q000502:physiology*; D011963:Receptors, GABA-A / Q000502:physiology*; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
chemical_list: D011954:Receptors, Dopamine; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid