Xiao Nong, Li Shizhi, Zhang Xiaoping, Chen Siyuan
Department of Neurology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Neurosci Lett. 2008 Apr 18;435(2):99-102. doi: 10.1016/j.neulet.2008.02.058. Epub 2008 Mar 4.
Study the effect of ephedrine on neural plasticity of hypoxic ischemic brain damaged (HIBD) in neonatal rats, and explore the underlying molecular mechanism.
60 Sprats suffered from HIBD (7 days old) were randomly divided into ephedrine group, D-amphetamine (D-AMPH) group, cytidine triphosphate (CTP) group, ganglioside (GM1) group, and spontaneous recovery group. Using immunohistochemical method to test the expression of growth-associated protein-43(GAP-43) and synaptophysin (SYP) on one side of hippocampal CA3 area, then, 4 weeks later, Morris Water Maze test was performed for five days.
(1) The expression levels of GAP-43 and SYP on hippocampal CA3 area in ephedrine group were higher than that in spontaneous recovery group (P<0.05). However, there was no statistical difference in ephedrine groups, CTP group, and D-AMPH group. (2) The average time of escape latency was significantly shorter in treating groups than that in spontaneous recovery group (P<0.05), and the frequency of original platform passing was higher than that in spontaneous recovery group (P<0.01). The average time of escape latency was longer in ephedrine group than that in GM1 group. The frequency of original platform passing was significantly less in ephedrine group than that in GM1 group, No statistical difference found in ephedrine groups, CTP group, and D-AMPH group.
Ephedrine may enhance memory, the abilities of spatial orientation and learning in HIBD rats. This protective effect may be associated with increasing synaptic connectivity, as assessed by increased expression of GAP-43 and SYP after HIBD. Ephedrine triggered similar protection against HIBD as treatment of D-AMPH and CTP. However, the amelioration of ability of spatial orientation, learning and memory by ephedrine on HIBD rats in later stage is slightly weaker than that by GM1, which may be related with ephedrine dosage.
研究麻黄碱对新生大鼠缺氧缺血性脑损伤（HIBD）神经可塑性的影响，并探讨其潜在的分子机制。
将60只HIBD（7日龄）大鼠随机分为麻黄碱组、右旋苯丙胺（D-AMPH）组、三磷酸胞苷（CTP）组、神经节苷脂（GM1）组和自然恢复组。采用免疫组织化学方法检测海马CA3区一侧生长相关蛋白-43（GAP-43）和突触素（SYP）的表达，4周后进行为期5天的Morris水迷宫试验。
（1）麻黄碱组海马CA3区GAP-43和SYP的表达水平高于自然恢复组（P<0.05）。然而，麻黄碱组、CTP组和D-AMPH组之间无统计学差异。（2）治疗组逃避潜伏期的平均时间显著短于自然恢复组（P<0.05），原平台穿越频率高于自然恢复组（P<0.01）。麻黄碱组逃避潜伏期的平均时间长于GM1组。麻黄碱组原平台穿越频率显著低于GM1组，麻黄碱组、CTP组和D-AMPH组之间无统计学差异。
麻黄碱可能增强HIBD大鼠的记忆、空间定向和学习能力。这种保护作用可能与增加突触连接性有关，HIBD后GAP-43和SYP表达增加可评估这一点。麻黄碱对HIBD的保护作用与D-AMPH和CTP治疗相似。然而，麻黄碱对HIBD大鼠后期空间定向、学习和记忆能力的改善略弱于GM1，这可能与麻黄碱剂量有关。
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