Brain γ-Aminobutyric Acid Abnormality in Tardive Dyskinesia: Reduction in Cerebrospinal Fluid GABA Levels and Therapeutic Response to GABA Agonist Treatment

G. K. Thaker, C. A. Tamminga, L. D. Alphs, J. Lafferman, T. N. Ferraro, T. A. Hare

Research output: Contribution to journalArticle

101 Scopus citations

Abstract

A double-blind, placebo-controlled trial of γ-vinyl γ-aminobutyric acid (GVG) and 4,5,6,7-tetrahydroisoxazolo-(5,4-c) pyridine-3-ol (THIP) was carried out in drug-free schizophrenic patients with tardive dyskinesia. A significant decrease in dyskinetic symptoms occurred with the administration of GVG, associated with a twofold increase in cerebrospinal fluid levels of GABA; THIP produced a more moderate, yet consistent decrease in the involuntary movements. A pathophysiologic role for γ-aminobutyric acid (GABA)-mediated neuronal transmission in tardive dyskinesia was explored by analyzing cerebrospinal fluid GABA concentrations in drugfree schizophrenic patients with and without tardive dyskinesia. A significant reduction in cerebrospinal fluid levels of GABA was observed in the dyskinetic schizophrenics compared with the nondyskinetic controls. These data compliment a growing body of experimental evidence suggesting a critical role for GABA-ergic neurons in the pathophysiology of tardive dyskinesia.

Original languageEnglish (US)
Pages (from-to)522-529
Number of pages8
JournalArchives of General Psychiatry
Volume44
Issue number6
DOIs
StatePublished - Jun 1987

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Psychiatry and Mental health

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