17β-estradiol treatment following permanent focal ischemia does not influence recovery of sensorimotor function
17β-estradiol treatment following permanent focal ischemia does not influence recovery of sensorimotor function
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DOI：
10.1016/j.nbd.2006.04.009
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发表时间：
2006-09-01
影响因子：
6.1
通讯作者：
Macrae, I. Mhairi
中科院分区：
文献类型：
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作者：
Farr, Tracy D.;Carswell, Hilary V. O.;Macrae, I. Mhairi
开发有助于中风后恢复的疗法至关重要。雌性激素 17 β-雌二醇已被证明可以促进突触发生；本研究的目的是尝试利用这些机制促进梗塞周围区域的修复和恢复。大鼠被切除卵巢，测试感觉运动功能，并对大脑中动脉永久闭塞（MCAO）。使用 MRI 计算梗塞体积，并且在植入 17 β-雌二醇或安慰剂颗粒之前，所有动物的损伤是相同的。对动物进行 28 天的功能恢复测试，并对组织进行突触标记突触蛋白免疫组织化学处理。中风引起了显着的行为缺陷，这种缺陷持续了 28 天，并且 17 个 β-雌二醇治疗组和安慰剂治疗组之间没有显着差异。在梗死周围皮质或树突 CA1 参考区域中，组间突触蛋白免疫染色没有差异。总之，中风后给予 17 β-雌二醇治疗不会影响功能恢复或突触发生。 (c) 2006 Elsevier Inc. 保留所有权利。
The development of therapy to aid poststroke recovery is essential. The female hormone 17 beta-estradiol has been shown to promote synaptogenesis; the purpose of this study was to attempt to harness these mechanisms to promote repair and recovery in the peri-infarct zone. Rats were ovariectomized, tested for sensorimotor function, and the middle cerebral artery permanently occluded (MCAO). Infarct volumes were calculated using MRI, and damage was equivalent in all animals prior to implantation of either 17 beta-estradiol or placebo pellets. Animals were tested for functional recovery for 28 days and tissue processed for synaptic marker syntaxin immunohistochemistry. The stroke induced a significant behavioral deficit, which persisted out to 28 days, and was not significantly different between 17 beta-estradiol and placebo treatment groups. There was no difference in syntaxin immunostaining between groups in either the peri-infarct cortex or in the dendritic CA1 reference region. In conclusion, 17 beta-estradiol treatment, delivered poststroke, did not influence recovery of function or synaptogenesis. (c) 2006 Elsevier Inc. All rights reserved .