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lüll Model generation and testing to probe neural circuitry in the cingulate cortex of postmortem schizophrenic brain Benes FMSchizophr Bull 1998[]; 24 (2): 219-30In the past decade, there has been increased interest in whether discreet alterations of neural circuitry might play a role in the pathophysiology of schizophrenia. In the absence of a readily identifiable histopathology, a variety of sophisticated neurobiological approaches is being applied to the study of this disorder. In one series of investigations, subtle abnormalities have been detected in the anterior cingulate cortex-layer II (ACCx-II) of schizophrenia patients. One of these studies suggested a reduction of nonpyramidal neurons in schizophrenia patients, and it was postulated that this change could give rise to a relative increase of dopaminergic inputs to the remaining gamma-aminobutyric acid (GABA) cells. Although empiric evidence in support of this hypothesis was obtained, a subsequent post hoc analysis, described in this report, has suggested that this change could have occurred irrespective of whether GABA cells are reduced in number. A shift of cortical dopamine afferents from pyramidal to nonpyramidal neurons in ACCx-II seems to provide a more plausible explanation for such a "miswiring." These findings support critical use of model generation and testing as powerful tools for unraveling the nature of altered neural circuitry in postmortem schizophrenic brain.|*Models, Neurological[MESH]|*Research Design/trends[MESH]|Autopsy/methods[MESH]|Brain/growth & development/pathology/physiopathology[MESH]|Cell Count[MESH]|Gyrus Cinguli/growth & development/*pathology/physiopathology[MESH]|Humans[MESH]|Neural Pathways/growth & development/pathology/physiopathology[MESH]|Neurons/cytology[MESH]|Pyramidal Cells/physiopathology[MESH]|Receptors, Dopamine/physiology[MESH]|Receptors, GABA/physiology[MESH]|Schizophrenia/*pathology/physiopathology[MESH] |