Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine
Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine
复制标题
通过胶质肌酸预防铵引起的轴突生长损伤
作者：
O. Braissant;H. Henry;A. Villard;M. Zurich;M. Loup;B. Eilers;Gianni Parlascino;E. Matter;O. Boulat;P. Honegger;C. Bachmann
新生儿和婴儿的高氨血症会影响大脑发育并导致智力迟钝。我们报告，铵损害胆碱能轴突的生长和改变的定位和磷酸化的中间神经丝蛋白在大鼠重组脑细胞原代培养。这种作用仅限于早期成熟阶段，但在突触发生后不发生。暴露于NH4Cl会降低细胞内肌酸、磷酸肌酸和ADP。我们证明，肌酸cotreatment保护轴突从铵的毒性作用，虽然这并没有恢复高能量磷酸盐。肌酸的保护作用依赖于胶质细胞。我们的研究结果表明，应评估有效维持高血氨新生儿和婴儿CNS肌酸浓度的方法，以防止轴突生成受损和不可逆的脑损伤。
Hyperammonemia in neonates and infants affects brain development and causes mental retardation. We report that ammonium impaired cholinergic axonal growth and altered localization and phosphorylation of intermediate neurofilament protein in rat reaggregated brain cell primary cultures. This effect was restricted to the phase of early maturation but did not occur after synaptogenesis. Exposure to NH4Cl decreased intracellular creatine, phosphocreatine, and ADP. We demonstrate that creatine cotreatment protected axons from ammonium toxic effects, although this did not restore high-energy phosphates. The protection by creatine was glial cell-dependent. Our findings suggest that the means to efficiently sustain CNS creatine concentration in hyperammonemic neonates and infants should be assessed to prevent impairment of axonogenesis and irreversible brain damage.
缺氧发育的大鼠大脑中磷酸肌酸和 ATP 的调节。
DOI：
10.1016/0165-3806(94)00213-j
发表时间：
1995
期刊：
Brain research. Developmental brain research
影响因子：
--
作者：
Tsuji,M;Allred,E;Jensen,F;Holtzman,D
通讯作者：
Holtzman,D
胎儿神经移植物中的细胞骨架蛋白免疫表达：磷酸化和非磷酸化神经丝蛋白和微管相关蛋白 2 (MAP-2) 的分布。
影响因子：
3.3
作者：
Rosenstein,JM;Krum,JM
通讯作者：
Krum,JM