Minocycline does not inhibit microglia proliferation or neuronal regeneration in the facial nucleus following crush injury

被引:22
作者
Fendrick, SE [1 ]
Miller, KR [1 ]
Streit, WJ [1 ]
机构
[1] Univ Florida, Dept Neurosci, Gainesville, FL 32610 USA
关键词
minocycline; H-3-thymidine; fluorogold;
D O I
10.1016/j.neulet.2005.05.047
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Minocycline is thought to be neuroprotective by inhibiting neuroinflammation (microglial activation) associated with neurodegenerative diseases. In this study we investigated the effect of minocycline specifically on microglial mitotic activity and neuronal regeneration within the facial nucleus following a nerve crush injury. Proliferation was measured by labeling the dividing microglia with H-3-thymidine and quantifying labeled cells throughout the facial nucleus on days 2, 3 and 4 post-axotomy. Regeneration patterns of the axotomized motoneurons were studied by labeling regenerating neurons with fluorogold at 7, 14 and 21 days post-axotomy. No significant difference was found between minocycline treated and control rats when comparing the 3H-thymidine labeled microglial cells or fluorogold labeled neurons at these post-injury time points. The findings show that microglia maintain the ability to become activated in vivo even in the presence of high levels of minocycline. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:220 / 223
页数:4
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