COMPARISON OF GLUTAMATE AND GAMMA-AMINOBUTYRIC-ACID UPTAKE BINDING-SITES IN FRONTAL AND TEMPORAL LOBES IN SCHIZOPHRENIA

Background: Theories of schizophrenia proposing deficiences of amino a cid [glutamate, gamma-aminobutyric acid (GABA)] neurons are in accord with the observed temporal lobe pathology of the disease rather than w ith the newer theory of glutamate hyperinnervation and hyperfunction i n areas of prefrontal cortex. This study addresses the issue by measur ing specific uptake sites as indices of glutamatergic and GABAergic ne uron densities in frontal and temporal lobes. Methods: Frontal cortex (six areas) and temporal lobe (six areas of cortex, amygdala, and hipp ocampus) were dissected from 19 control autopsy brains and 12 brains f rom neuroleptic drug-treated schizophrenic patients. Groups had simila r ages, postmortem intervals, and storage times. Membranes, prepared f rom tissue homogenates, were incubated with D-[H-3]aspartate to measur e neuronal and glial glutamate uptake site binding in 14 areas and wit h [H-3]nipecotic acid to measure neuronal GABA uptake site binding in II areas. Results: Glutamate and GABA uptake sites were not reduced in prefrontal and temporal areas. Instead, we found small increases in g lutamate uptake sites in prefrontal areas. Some tendency toward increa sed GABA uptake sites were not disease-related. Conclusions: Our findi ngs concur with other studies that propose locally overabundant glutam ate systems in prefrontal cortex in schizophrenia. Losses of amino aci d neurons do not accompany the temporal lobe pathology. (C) 1998 Socie ty of Biological Psychiatry.