ABSENCE OF BASAL GANGLIA AMINO-ACID NEURON DEFICITS IN SCHIZOPHRENIA IN 3 COLLECTIONS OF BRAINS

Amino acid (glutamatergic, GABAergic) neuron deficiency, theories of s chizophrenia offer plausible explanations of pathogenesis. However, re ports of disease-related reductions in amino acid synthesizing enzymes in postmortem brains are contradictory. We measured neuronal uptake s ites for gamma-aminobutyric acid (GABA; [H-3]nipecotic acid binding) a nd nerve terminal/glial uptake sites for L-glutamate (D-[H-3]aspartate binding) in three independent groups of post-mortem brains from patie nts with schizophrenia and control subjects. Measurements were also ma de of the phencyclidine site of the glutamate iv-methyl-D-aspartate (N MDA) receptor. Samples from patients showed no reductions in the bindi ng of [H-3]nipecotic acid or D -[H-3]aspartate in caudate, putamen or globus pallidus. On the contrary, some increased binding of both ligan ds was observed in patients in many comparisons with controls. There w ere no clear-cut changes in NMDA receptor binding. The most consistent change in the brain sets was increased [H-3]nipecotic acid binding in caudate-putanen. This could be due to neuroleptic treatment. The find ings produce no evidence that schizophrenia involves major loss of GAB A neuron terminals in the basal ganglia or losses of corticostriatal g lutamatergic projections. (C) 1998 Elsevier Science B.V. All rights re served.