Sundman-Eriksson Ingrid, Allard Per
Division of Psychiatry, Department of Clinical Sciences, Umeå University, S-901 85 Umeå, Sweden.
J Affect Disord. 2002 Sep;71(1-3):29-33. doi: 10.1016/s0165-0327(01)00349-4.
In depressive disorders, alterations of GABA concentrations and number of postsynaptic GABA related receptor binding sites, as well as antidepressant effects exerted by GABA agonists, suggest a pathogenetic involvement of the GABA system.
The binding of the presynaptic GABA ligand [(3)H]tiagabine to GABA transporter-1 (GAT-1) was studied in post mortem human frontal cortex and cingulate gyrus from 13 suicide victims and 19 controls without known neurological or psychiatric disorder.
No differences were found between the suicide victims and the controls with regard to the number of [(3)H]tiagabine binding sites (B(max)) or apparent affinity (K(d)).
The study was limited to two brain regions.
Findings in other studies of alterations in the GABA system in depression seem according to the present results not to be associated with significant changes in the GABA uptake binding sites in the regions investigated.