Increased [(3)H]tiagabine binding to GAT-1 in the cingulate cortex in schizophrenia.

Postmortem samples from individuals with schizophrenia (n = 13) and control subjects (n = 10) were investigated for binding of (3)H]tiagabine to GABA transporter-1 GAT-1. The binding was analyzed in the cingulate cortex and the caudate nucleus. There were no differences in binding affinity between the groups in any of the investigated areas. The maximum number of binding sites (B(max)) was elevated in the schizophrenic cingulate cortex compared to controls (1,264 +/- 96 vs. 860 +/- 123 fmol/mg of protein). The B(max) in the caudate nucleus for schizophrenics (426 +/- 40 fmol/mg of protein) was the same as for controls (495 +/- 69 fmol/mg of protein). The increase in GAT-1 in schizophrenia could be explained by a modulatory upregulation in the cingulate cortex.