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Up-regulation of GABAA receptors in the post-mortem brain has been reported in schizophrenia. This increase may explain the role of GABA in the pathophysiology of schizophrenia. GABAA receptor subunit mRNA levels were analyzed by competitive quantitative RT-PCR in normal human striatal tissue from 10 control subjects. The same samples were used to investigate subunit mRNA levels in the hippocampus and prefrontal cortex (PFC), two other brain regions frequently considered as putative sites of pathophysiology in schizophrenia. Quantitative RT-PCR results were compared with those of GABAA receptor subunit binding sites assessed with ligand autoradiography using [3H]muscimol. The distribution of [3H]muscimol binding in the human striatum was similar to those reported in rodents and primates. In the human striatum, [3H]muscimol binding was only 2.6-fold higher in the putamen than in the caudate nucleus. [3H]Muscimol binding was lower in the putamen than in the caudate nucleus in agreement with the 2-fold increase in GABAA receptor subunit mRNA in the latter compared with the putamen. [3H]Muscimol binding in the human PFC was also low compared with rat and macaque. The low [3H]muscimol binding in the PFC was associated with low levels of GABAA receptor subunit mRNA. The limited distribution of [3H]muscimol binding in the human striatum is in agreement with the large body of functional data indicating predominant extrasynaptic GABAA receptor localization in this region. The very low levels of [3H]muscimol binding in the PFC indicate low levels of alpha1, alpha6, and beta2 mRNA and/or low muscimol binding affinity compared with those reported in rodents and primates. Our results suggest