Otani Naoki, Nawashiro Hiroshi, Fukui Shinji, Ooigawa Hidetoshi, Ohsumi Atsushi, Toyooka Terushige, Shima Katsuji, Gomi Hiroshi, Brenner Michael
Department of Neurosurgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.
J Clin Neurosci. 2006 Nov;13(9):934-8. doi: 10.1016/j.jocn.2005.10.018.
Astrocytes perform a variety of functions in the adult central nervous system. Recent evidence suggests that the upregulation of glial fibrillary acidic protein (GFAP), an astrocyte-specific intermediate filament component, is a biological marker of neurotoxicity after cerebral injury. We herein compared the response to traumatic brain injury or kainic acid (KA)-induced neurotoxicity in GFAP knockout (GFAP-KO) and wild-type (WT) mice. Seventy-two hours after injury, all GFAP-KO mice showed hippocampal CA3 neurodegeneration, whereas WT mice did not show neurodegeneration. Seventy-two hours after KA administration, GFAP-KO mice were more susceptible to KA-induced seizures and had an increased number of pyknotic damaged CA3 neurons than did WT mice. These results indicate that GFAP plays a crucial role in pyramidal neuronal survival after injury or KA-induced neurotoxicity.
星形胶质细胞在成体中枢神经系统中发挥多种功能。最近的证据表明，胶质纤维酸性蛋白（GFAP）作为一种星形胶质细胞特异性中间丝成分，其表达上调是脑损伤后神经毒性的生物学标志物。我们在此比较了GFAP基因敲除（GFAP-KO）小鼠和野生型（WT）小鼠对创伤性脑损伤或 kainic 酸（KA）诱导的神经毒性的反应。损伤后72小时，所有GFAP-KO小鼠均出现海马CA3区神经退行性变，而WT小鼠未出现神经退行性变。给予KA后72小时，GFAP-KO小鼠比WT小鼠更易发生KA诱导的癫痫发作，且固缩受损的CA3神经元数量增加。这些结果表明，GFAP在损伤或KA诱导的神经毒性后锥体神经元存活中起关键作用。
