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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Delayed treatment with monoclonal antibody IN-1 1 week after stroke results in recovery of function and corticorubral plasticity in adult rats.
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Delayed treatment with monoclonal antibody IN-1 1 week after stroke results in recovery of function and corticorubral plasticity in adult rats.

机译：脑卒中后1周延迟使用单克隆抗体IN-1进行治疗可导致成年大鼠功能恢复和皮层可塑性恢复。

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Neuronal death due to ischemic stroke results in permanent deficits in sensory, language, and motor functions. The growth-restrictive environment of the adult central nervous system (CNS) is an obstacle to functional recovery after stroke and other CNS injuries. In this regard, Nogo-A is a potent neurite growth-inhibitory protein known to restrict neuronal plasticity in adults. Previously, we have found that treatment with monoclonal antibody (mAb) IN-1 to neutralize Nogo-A immediately after stroke enhanced motor cortico-efferent plasticity and recovery of skilled forelimb function in rats. However, immediate treatment for stroke is often not clinically feasible. Thus, the present study was undertaken to determine whether cortico-efferent plasticity and functional recovery would occur if treatment with mAb IN-1 was delayed 1 week after stroke. Adult rats were trained on a forelimb-reaching task, and the middle cerebral artery was occluded to induce focal cerebral ischemia to the forelimb sensorimotor cortex. After 1 week, animals received mAb IN-1 treatment, control antibody, or no treatment, and were tested for 9 more weeks. To assess cortico-efferent plasticity, the sensorimotor cortex opposite the stroke lesion was injected with an anterograde neuroanatomical tracer. Behavioral analysis demonstrated a recovery of skilled forelimb function, and anatomical studies revealed neuroplasticity at the level of the red nucleus in animals treated with mAb IN-1, thus demonstrating the efficacy of this treatment even if administered 1 week after stroke.
机译：缺血性中风导致的神经元死亡导致感觉，语言和运动功能永久性缺陷。成人中枢神经系统（CNS）的生长受限环境是中风和其他CNS损伤后功能恢复的障碍。在这方面，Nogo-A是一种有效的抑制神经突生长的蛋白，已知会限制成人的神经元可塑性。以前，我们发现在中风后立即用单克隆抗体（mAb）IN-1处理以中和Nogo-A可以增强大鼠运动皮质的可塑性和恢复熟练的前肢功能。但是，立即治疗中风通常在临床上不可行。因此，本研究旨在确定如果卒中后1周延迟使用mAb IN-1进行治疗，是否会发生皮质有效的可塑性和功能恢复。对成年大鼠进行前肢伸展训练，并闭塞大脑中动脉以诱导前肢感觉运动皮层局灶性脑缺血。 1周后，动物接受mAb IN-1处理，对照抗体或不进行处理，并再测试9周。为了评估皮质有效的可塑性，向顺风病变对面的感觉运动皮层注射顺行神经解剖示踪剂。行为分析表明，熟练的前肢功能已恢复，并且解剖学研究显示，在用mAb IN-1治疗的动物中，红色核水平具有神经可塑性，因此即使在卒中后1周给药，也证明了该治疗的有效性。

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