Enriched environment downregulates macrophage migration inhibitory factor and increases parvalbumin in the brain following experimental stroke
Enriched environment downregulates macrophage migration inhibitory factor and increases parvalbumin in the brain following experimental stroke
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DOI：
10.1016/j.nbd.2010.09.015
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发表时间：
2011-02-01
影响因子：
6.1
通讯作者：
Wieloch, Tadeusz
中科院分区：
文献类型：
--
作者：
Inacio, Ana R.;Ruscher, Karsten;Wieloch, Tadeusz
在实验性中风后将啮齿动物安置在丰富的环境（EE）中可促进神经恢复。了解潜在的神经线索可以为改善中风康复提供基础。我们研究了脑巨噬细胞移动抑制因子（MIF）对大鼠永久性大脑中动脉闭塞（pMCAo）后功能恢复的作用。在大脑皮层中，MIF主要存在于神经元中，特别是在小白蛋白中间神经元中。在pMCAo后，MIF在梗死核心周围增加，在那里它位于神经元和星形胶质细胞。在pMCAo后，将大鼠置于EE中导致脑梗死区MIF蛋白水平降低，同时伴随着小白蛋白免疫反应性中间神经元的增加。我们的数据表明，MIF是参与大脑可塑性的信号网络的一部分，升高的神经元和/或星形胶质细胞MIF水平抑制中风后感觉运动功能的恢复。下调MIF可能成为促进脑卒中后恢复的一种新的治疗方法。(C)2010年爱思唯尔公司All rights reserved.
Housing rodents in an enriched environment (EE) following experimental stroke enhances neurological recovery. Understanding the underlying neural cues may provide the basis for improving stroke rehabilitation. We studied the contribution of brain macrophage migration inhibitory factor (MIF) to functional recovery after permanent middle cerebral artery occlusion (pMCAo) in rats. In the cerebral cortex, MIF is predominantly found in neurons, particularly in parvalbumin interneurons. Following pMCAo, MIF increases around the infarct core, where it is located to neurons and astrocytes. Housing rats in an EE after pMCAo resulted in a decrease of MIF protein levels in pen-infarct areas, which was accompanied by an increase in parvalbumin immunoreactive interneurons. Our data suggest that MIF is part of a signaling network involved in brain plasticity, and elevated neuronal and/or astrocytic MIF levels repress the recovery of sensory-motor function after stroke. Downregulating MIF could constitute a new therapeutic approach to promote recovery after stroke. (C) 2010 Elsevier Inc. All rights reserved.