Farr Tracy D, Carswell Hilary V O, Gallagher Lindsay, Condon Barrie, Fagan Andrew J, Mullin Jim, Macrae I Mhairi
7TMRI Facility and Wellcome Surgical Institute, Division of Clinical Neuroscience, University of Glasgow, Garscube Estate, Bearsden Road, Glasgow, Scotland G61 1QH, UK.
Neurobiol Dis. 2006 Sep;23(3):552-62. doi: 10.1016/j.nbd.2006.04.009. Epub 2006 Jun 8.
The development of therapy to aid poststroke recovery is essential. The female hormone 17beta-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 17beta-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 17beta-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, 17beta-estradiol treatment, delivered poststroke, did not influence recovery of function or synaptogenesis.
开发有助于中风后恢复的疗法至关重要。已证明女性激素17β-雌二醇可促进突触形成；本研究的目的是试图利用这些机制促进梗死周围区域的修复和恢复。对大鼠进行卵巢切除，测试其感觉运动功能，然后永久性闭塞大脑中动脉（MCAO）。使用MRI计算梗死体积，在植入17β-雌二醇或安慰剂微丸之前，所有动物的损伤情况均相同。对动物进行28天的功能恢复测试，并对组织进行突触标记物 syntaxin免疫组织化学处理。中风导致了显著的行为缺陷，这种缺陷持续到28天，在17β-雌二醇和安慰剂治疗组之间没有显著差异。在梗死周围皮质或树突状CA1参考区域，两组之间的syntaxin免疫染色没有差异。总之，中风后给予17β-雌二醇治疗，并不影响功能恢复或突触形成。
