Yamada K, Goto S, Oyama T, Inoue N, Nagahiro S, Ushio Y
Department of Neurosurgery, Kumamoto University Medical School, Japan.
Acta Neuropathol. 1994;88(6):553-7. doi: 10.1007/BF00296492.
Immunohistochemistry was used to investigate the induction of growth-associated protein GAP43/B-50 in the astrocytes of rat cerebrum in vivo following ischemic injury produced by 30 min of transient middle cerebral artery occlusion. Three days after operation, GAP43 immunoreactivity first appeared in some astrocytic populations surrounding the infarcted lesion. Induction of GAP43 in those astrocytes persisted for up to 14 days and disappeared at 30 days postoperation. Double-immunofluorescence staining confirmed that the GAP43-immunoreactive astrocytes examined were all positive for glial fibrillary acidic protein. Our present data suggest that certain astrocytes could be induced to synthesize GAP43 in vivo in response to an ischemic insult in adult rats.
采用免疫组织化学方法,研究成年大鼠大脑中动脉短暂闭塞30分钟所致缺血性损伤后,体内大鼠大脑星形胶质细胞中生长相关蛋白GAP43/B-50的诱导情况。术后3天,GAP43免疫反应性首次出现在梗死灶周围的一些星形胶质细胞群体中。这些星形胶质细胞中GAP43的诱导持续长达14天,并在术后30天消失。双重免疫荧光染色证实,所检测的GAP43免疫反应性星形胶质细胞对胶质纤维酸性蛋白均呈阳性。我们目前的数据表明,成年大鼠体内某些星形胶质细胞可因缺血性损伤而被诱导合成GAP43。