The Role of Endogenous Neurogenesis in Functional Recovery and Motor Map Reorganization Induced by Rehabilitative Therapy after Stroke in Rats.
The Role of Endogenous Neurogenesis in Functional Recovery and Motor Map Reorganization Induced by Rehabilitative Therapy after Stroke in Rats.
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DOI：
10.1016/j.jstrokecerebrovasdis.2016.09.016
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发表时间：
2017-02
期刊：
影响因子：
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通讯作者：
T. Shiromoto;N. Okabe;F. Lu;Emi Maruyama-Nakamura;Naoyuki Himi;K. Narita;Y. Yagita;K. Kimura;O. Miyamoto
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文献类型：
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作者：
T. Shiromoto;N. Okabe;F. Lu;Emi Maruyama-Nakamura;Naoyuki Himi;K. Narita;Y. Yagita;K. Kimura;O. Miyamoto
内源性神经发生与卒中后功能恢复有关，但其在恢复过程中的作用尚不清楚。本研究旨在阐明内源性神经发生的作用，在功能恢复和运动地图重组引起的康复治疗中风后，通过使用脑缺血（CI）大鼠模型。首先，我们研究了康复治疗对功能恢复和运动地图重组的影响，使用熟练的前肢达到测试和皮质内微刺激。接下来，使用相同的方法，我们研究了如何改变运动地图重组时，内源性神经发生后，中风被抑制胞嘧啶-β-D-阿拉伯呋喃糖苷（Ara-C）。结果诱导中风后4周的康复治疗显着改善功能恢复和扩大喙前肢区（RFA）。与媒介物相比，中风后4-10天的脑室内Ara-C施用显著抑制内源性神经发生，但似乎不影响非神经细胞（例如，小胶质细胞、星形胶质细胞和血管内皮细胞）。通过Ara-C管理抑制内源性神经发生显着抑制（约50%低于车辆）功能恢复和RFA扩张（约33%的车辆）诱导康复治疗后CI.ConclusionsAfter CI，抑制内源性神经发生抑制康复治疗的功能和解剖标志物。这些结果表明，内源性神经发生有助于功能恢复后CI相关的康复治疗，可能通过其促进运动地图重组，虽然其他额外的作用不能排除。
Background and ObjectiveEndogenous neurogenesis is associated with functional recovery after stroke, but the roles it plays in such recovery processes are unknown. This study aims to clarify the roles of endogenous neurogenesis in functional recovery and motor map reorganization induced by rehabilitative therapy after stroke by using a rat model of cerebral ischemia (CI).MethodsIschemia was induced via photothrombosis in the caudal forelimb area of the rat cortex. First, we examined the effect of rehabilitative therapy on functional recovery and motor map reorganization, using the skilled forelimb reaching test and intracortical microstimulation. Next, using the same approaches, we examined how motor map reorganization changed when endogenous neurogenesis after stroke was inhibited by cytosine-β-d-arabinofuranoside (Ara-C).ResultsRehabilitative therapy for 4 weeks after the induction of stroke significantly improved functional recovery and expanded the rostral forelimb area (RFA). Intraventricular Ara-C administration for 4-10 days after stroke significantly suppressed endogenous neurogenesis compared to vehicle, but did not appear to influence non-neural cells (e.g., microglia, astrocytes, and vascular endothelial cells). Suppressing endogenous neurogenesis via Ara-C administration significantly inhibited (~50% less than vehicle) functional recovery and RFA expansion (~33% of vehicle) induced by rehabilitative therapy after CI.ConclusionsAfter CI, inhibition of endogenous neurogenesis suppressed both the functional and anatomical markers of rehabilitative therapy. These results suggest that endogenous neurogenesis contributes to functional recovery after CI related to rehabilitative therapy, possibly through its promotion of motor map reorganization, although other additional roles cannot be ruled out.