Brain Excitability in Stroke The Yin and Yang of Stroke Progression
Brain Excitability in Stroke The Yin and Yang of Stroke Progression
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DOI：
10.1001/archneurol.2011.1175
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发表时间：
2012-02-01
影响因子：
--
通讯作者：
Carmichael, S. Thomas
中科院分区：
文献类型：
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作者：
Carmichael, S. Thomas
目前没有中风恢复的药物治疗。在动物模型和人类中风的恢复过程中，已经确定了生理可塑性的原则。中风导致邻近梗塞周围皮层的生理脑地图丢失，然后在该区域重新绘制运动和感觉功能。梗死周围皮质功能的重新映射与恢复密切相关。最近的研究表明，中风在邻近梗死的神经元回路中产生异常的兴奋性条件，这可能是大脑重新映射和恢复过程的基质。中风导致梗死周围运动皮层的低兴奋性，这源于神经元上的强直性γ-氨基丁酸活性增加。逆转这种γ-氨基丁酸信号的药物可以促进中风后的恢复。中风还在中风事件之后很久增加了梗塞周围皮层中谷氨酸受体信号传导的敏感性，并且刺激梗塞周围皮层中的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸盐谷氨酸受体促进中风后的恢复。阻断紧张性γ-氨基丁酸电流和刺激α-氨基-3-羟基-5-甲基-4-异恶唑-丙酸酯受体都能促进卒中后的恢复，但起始时间较晚，超过梗死后3 - 5天。中风后梗死周围皮层神经元回路兴奋性的这些变化可能是中风后运动和感觉功能重新映射过程的基础，并可能确定新的治疗靶点以促进中风恢复。神经弓2012;69（2）：161-167. 2011年10月10日在线发布。doi：10.1001/archneurol.2011.1175
There is no current medical therapy for stroke recovery. Principles of physiological plasticity have been identified during recovery in both animal models and human stroke. Stroke produces a loss of physiological brain maps in adjacent peri-infarct cortex and then a remapping of motor and sensory functions in this region. This remapping of function in peri-infarct cortex correlates closely with recovery. Recent studies have shown that the stroke produces abnormal conditions of excitability in neuronal circuits adjacent to the infarct that may be the substrate for this process of brain remapping and recovery. Stroke causes a hypo-excitability in peri-infarct motor cortex that stems from increased tonic gamma-aminobutyric acid activity onto neurons. Drugs that reverse this gamma-aminobutyric acid signaling promote recovery after stroke. Stroke also increases the sensitivity of glutamate receptor signaling in peri-infarct cortex well after the stroke event, and stimulating alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate glutamate receptors in peri-infarct cortex promotes recovery after stroke. Both blocking tonic gamma-aminobutyric acid currents and stimulating alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors promote recovery after stroke when initiated at quite a delay, more than 3 to 5 days after the infarct. These changes in the excitability of neuronal circuits in peri-infarct cortex after stroke may underlie the process of remapping motor and sensory function after stroke and may identify new therapeutic targets to promote stroke recovery. Arch Neurol. 2012;69(2):161-167. Published online October 10, 2011. doi:10.1001/archneurol.2011.1175