2019 Volume 30 Issue 3 Pages 108-113
Increased density of white matter neurons (WMNs) in the neocortex has been reported as one of the reproducible histological changes in postmortem brains from subpopulations of patients with schizophrenia and autistic spectrum disorder (ASD) . Although researchers have thought that the changes are caused by migration defects of the neocortical neurons or failed apoptosis of the subplate (SP) neurons, no discrete conclusions have been arrived at yet. If the increase in the density of the WMNs were caused by failed apoptosis of the SP neurons, alterations of the SP neurons might underlie the presumed abnormal cortical wiring in schizophrenic or ASD brains, since the SP plays a key role in the establishment of neocortical connectivity during development. On the other hand, recent experimental mouse studies have demonstrated that either genetic or environmental factors that enhance the risk of neuropsychiatric disorders during development could cause neuronal migration deficits and altered distribution of the neocortical neurons in the white matter. In our newly established experimental mouse models, abnormal neocortical wiring was observed when the number of neocortical WMNs was artificially increased. Further investigations of the brains of both human patients and animal models will contribute to a precise elucidation of the pathophysiological mechanisms underlying the increased density of the neocortical WMNs in the subpopulations of schizophrenia/ASD patients.
