Injury and diseases of the nervous system can induce astrocytes to form ten
acious glial scars. We induced focal cortical freeze-lesions in neonatal ra
ts and examined scars histologically and electrophysiologically in tissue s
lices isolated 2-3 weeks after lesioning. Lesions displayed marked gliosis,
characterized by upregulation of GFAP labeling. Reactive astrocytes surrou
nding the scar showed marked hypertrophy, enlarged cell bodies and extended
processes frequently terminating with endfeet-like structures on blood ves
sels. These reactive astrocytes showed enhanced expression of inwardly rect
ifying K+ (K-IR) channels, widely believed to be an important pathway for a
strocytic K+ buffering. These results suggest that a subpopulation of react
ive astrocytes along a glial scar might be instrumental in buffering K+ awa
y from the lesion. NeuroReport 11:3151-3155 (C) 2000 Lippincott Williams &
Wilkins.