The growth-associated protein GAP-43 is increased in the hippocampus and in the gyrus cinguli in schizophrenia

摘要: Schizophrenia is a common and severe psychiatric disorder of unknown etiology. Numerous neuropathological studies have found subtle structural changes in limbic structures, especially medial temporal lobe structures the gyrus cinguli. To test hypothesis that synaptic disturbances are involved pathogenesis schizophrenia, we studied growth-associated protein 43 (GAP-43), localized to presynaptic terminals, suggested be establishment remodeling connections, postmortem brain tissue, using quantitative Western blotting immunohistochemistry. The material consisted tissue from 17 schizophrenics (80±11 yr), diagnosed according DSM-III-R criteria, 20 age-matched controls (75±13 yr). Quantitative analyses showed increased GAP-43 levels schizophrenic compared control brains, both hippocampus (2.43±0.78 vs 1.00±0.29; p<0.0001) cinguli (1.52±0.21 1.00±0.35; p<0.0001). Also by immuno-histochemistry, staining was with throughout all layers hippocampus. Anomalous sprouting reorganization, resultant “miswiring,” as well defect pruning been hypothesized pathogenetic factors schizophrenia. We suggest decreased density, whether caused disturbed development or damage/degeneration, may elicit reactive synaptogenesis (reflected an increase GAP-43), which functional anomalous. Synaptic pathology system importance psychotic symptoms