O'Callaghan J P, Seidler F J
Neurotoxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.
Neurosci Lett. 1992 Dec 14;148(1-2):105-8. doi: 10.1016/0304-3940(92)90815-o.
Mechanical injury to the brain results in enhanced immunostaining for glial fibrillary acidic protein (GFAP) that is markedly inhibited by difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase. In the current study, systemic exposure of mice to the dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), also increased GFAP but, unlike mechanical injury, this increase was not prevented by DFMO pretreatment. These results indicate that de novo polyamine biosynthesis is not obligatory for the MPTP-induced increase in GFAP. MPTP administration, unlike mechanical injury, does not disrupt the blood-brain barrier; thus, a role for polyamine biosynthesis in the astrocyte response to injury may be restricted to insults involving a compromised blood-brain barrier.
脑机械损伤会导致胶质纤维酸性蛋白（GFAP）免疫染色增强，而鸟氨酸脱羧酶的不可逆抑制剂二氟甲基鸟氨酸（DFMO）可显著抑制这种增强。在当前研究中，小鼠全身暴露于多巴胺能神经毒物1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）也会使GFAP增加，但与机械损伤不同的是，DFMO预处理并不能阻止这种增加。这些结果表明，从头合成多胺对于MPTP诱导的GFAP增加并非必需。与机械损伤不同，MPTP给药不会破坏血脑屏障；因此，多胺生物合成在星形胶质细胞对损伤的反应中的作用可能仅限于涉及血脑屏障受损的损伤。
