Dragunow M, de Castro D, Faull R L
Department of Pharmacology, School of Medicine, University of Auckland, New Zealand.
Brain Res. 1990 Sep 10;527(1):41-54. doi: 10.1016/0006-8993(90)91058-o.
Focal brain injury or perforant-path transections respectively led to an increase in the number of glial-fibrillary acidic protein (GFAP)-immunopositive astrocytes around the focal wound or in the terminal fields of the perforant path in the dentate molecular layer. This GFAP accumulation occurred 48-72 h after focal brain injury or perforant-path transection (wallerian degeneration). Focal brain injury also led to an accumulation of c-fos protein (Fos) in glial cells, ependyma and cells in the pia mater of the brain within 6 h of injury and this effect dissipated within 72 h. However, perforant-path lesions were not associated with accumulation of Fos in glial cells in the dentate molecular layer suggesting that c-fos induction in glial cells after injury is not necessary for GFAP accumulation. Induction of Fos in glia, ependyma and pia after focal brain injury may be associated with proliferation of these cells after injury.
局灶性脑损伤或穿通通路横断分别导致局灶性伤口周围或齿状分子层穿通通路终末区域胶质纤维酸性蛋白（GFAP）免疫阳性星形胶质细胞数量增加。这种GFAP积累发生在局灶性脑损伤或穿通通路横断（沃勒变性）后48 - 72小时。局灶性脑损伤还导致损伤后6小时内胶质细胞、室管膜和软脑膜细胞中c - fos蛋白（Fos）积累，且这种效应在72小时内消失。然而，穿通通路损伤与齿状分子层胶质细胞中Fos积累无关，这表明损伤后胶质细胞中c - fos诱导对于GFAP积累并非必要。局灶性脑损伤后胶质细胞、室管膜和软脑膜中Fos的诱导可能与损伤后这些细胞的增殖有关。
