Abstract
Injury and diseases of the nervous system can induce astrocytes to form tenacious glial scars. We induced focal cortical freeze-lesions in neonatal rats and examined scars histologically and electrophysiologically in tissue slices isolated 2-3 weeks after lesioning. Lesions displayed marked gliosis, characterized by upregulation of GFAP labeling. Reactive astrocytes surrounding the scar showed marked hypertrophy, enlarged cell bodies and extended processes frequently terminating with endfeet-like structures on blood vessels. These reactive astrocytes showed enhanced expression of inwardly rectifying K+ (K(IR)) channels, widely believed to be an important pathway for astrocytic K+ buffering. These results suggest that a subpopulation of reactive astrocytes along a glial scar might be instrumental in buffering K+ away from the lesion.
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