Diaschisis has been described as functional depression distant to the lesion. A variety of neuroscientific approaches have been used to investigate the mechanisms underlying
diaschisis. However, few studies have examined the pathological changes in
diaschisis at ultrastructural level. Here, we used a rat model of capsular
infarct that consistently produces
diaschisis in ipsilesional and contralesional motor and sensory cortices. To verify the occurrence of
diaschisis and monitor time-dependent changes in
diaschisis, we performed longitudinal 2-deoxy-2-[18F]-fluoro-
d-glucose microPET (FDG-microPET) study. We also used light and electron microscopy to identify the microscopic and ultrastructural changes at the
diaschisis site at 7, 14, and 21 days after capsular
infarct modeling (CIM). FDG-microPET showed the occurrence of
diaschisis after CIM. Light microscopic examinations revealed no significant histopathological changes at the
diaschisis site except a mild degree of reactive
astrogliosis. However, electron microscopy revealed swollen, hydropic degeneration of axial dendrites and axodendritic synapses, although the neuronal
soma (including nuclear
chromatin and cytoplasmic organelles) and myelinated axons were relatively well preserved up to 21 days after injury. Furthermore, number of axodendritic synapses was significantly decreased after CIM. These data indicate that a circumscribed subcortical white-matter lesion produces ultrastructural pathological changes related to the pathogenesis of
diaschisis.