GABA dysfunction in the pathophysiology of tardive dyskinesia.

C. A. Tamminga, G. K. Thaker, T. N. Chase

Research output: Contribution to journalArticle

13 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)122-127
Number of pages6
JournalPsychopharmacology. Supplementum
Volume2
StatePublished - 1985

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gamma-Aminobutyric Acid
Dopamine Receptors
Antipsychotic Agents
Hypersensitivity
Animal Models
Corpus Striatum
Basal Ganglia
Dopamine
Tardive Dyskinesia

ASJC Scopus subject areas

  • Medicine(all)

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GABA dysfunction in the pathophysiology of tardive dyskinesia. / Tamminga, C. A.; Thaker, G. K.; Chase, T. N.

In: Psychopharmacology. Supplementum, Vol. 2, 1985, p. 122-127.

Research output: Contribution to journalArticle

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