Brain dysgenesis in late onset schizophrenia (paraphrenia): Comparison with controls and patients with schizophrenia

Abstract

Recent postmortem studies have suggested that a defect of GABAergic neurotransmission might be p~esent in layer II of the anterior cingulate cortex (ACCxII) 10 SZs. To explore this possibility, an immunoperoxidase method has been developed to localize GADwIR terminals on PNs and NPs in layers II III V and VI of 12 normal controls (CONs) and 12 SZs matched for age and postmortem interval. The results showed no difference in the density of terminals on either cell type in any of the layers examined. When the SZs with and wit~out (N =2) neuroleptic exposure (CPZ) wer~ separately examm~d, the drug-free patients showed a 4010 higher terminal density on both PNs (p=O.044) and NPs (p=O.035) in layer II and on PNs in layer III. The fact that tbe density of terminals was significantly higher on NPs than on PNs in both CONs and SZs has suggested that the role of disinhibitory GABA activity may be more pronounced in human ACCx than was heretofore suspected. Overall, the results of ~s study are. in agreem~nt with the general view that defective GABAergJc modulation may playa role in ACCx-II of SZS, and that neuroleptic drugs may help to correct such an abnormality. Supported by MH00423, MH42261, MH31154 and MH31862.