Chondroitin sulfate proteoglycans have been shown to participate in the pathogenesis of neuronal damages in the injured adult central nervous system (CNS). Upregulated expression of
chondroitin sulfate proteoglycans has been reported around the injured sites and depletion of these
chondroitin sulfate proteoglycans brings about increased axonal regeneration in the injured adult CNS. To examine if
chondroitin sulfate proteoglycans are also involved in the pathologic process of
hypoxia-
ischemia in the neonatal brain, expressions of three
chondroitin sulfate proteoglycans,
neurocan,
phosphacan, and neuroglycan C, were examined in rat brains after neonatal
hypoxia-
ischemia. Hypoxic-ischemic rats were produced by ligating the right carotid artery of 7-day-old rats, followed by 8%
oxygen exposure. Western blot analysis revealed that in contrast to injured adult CNS, the amount of
neurocan was reduced 24 hr after
hypoxia in the neonatal hypoxic-ischemic cerebral hemisphere. The amounts of
phosphacan and neuroglycan C were also reduced significantly 24 hr after
hypoxia at the right injured cortex compared to those at the left cortex. Surprisingly, the immunohistologic staining for
phosphacan was conversely intensified both at 24 hr and 8 days after
hypoxia at the infarcted area. In addition, the habenula and fascicules retroflexus in the right cerebral hemisphere degenerated and became intensely immunostained with the anti-
phosphacan antibody shortly after
hypoxia. Hypoxic-ischemic insult may unmask
phosphacan epitopes at the injured sites, resulting in intensified immunostaining. Because intensified immunostaining for
neurocan and neuroglycan C was not observed, unmasking seems to be specific to
phosphacan among these three
chondroitin sulfate proteoglycans.