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A method for monitoring intra-cortical motor cortex responses in an animal model of ischemic stroke

机译:一种监测缺血性卒中动物模型中皮质型电机皮层反应的方法

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Neuroplasticity is believed to play a key role in functional recovery after stroke. Neuroplastic effects can be monitored at the cellular level via e.g. neurotransmitter assessment, but these studies require sacrifice of the animal. FMRI can be used to assess functional neuronal performance, but the spatial and temporal resolution is far from the single cell level. The objective was to establish an effective method for short-term analysis of single and multi-unit electrophysiological function before, during and after stroke. We instrumented one rat with a 16-ch array in the primary motor cortex (100 mum wire diameter) to monitor cortical activity. A bipolar cuff electrode was implanted around the Ulnar nerve in the contralateral forelimb to provide a controlled electrical stimulus input to the sensory-motor system. A 3 mm diameter ischemic infarct was created immediately posterior to the electrode array by light activation of a photosensitive dye (Rose Bengal, 1.3 mg/100 mg body weight) at the cortical surface. M1 activity in response to the peripheral electrical stimulus was recorded before, during and after the cortical ischemic infarct. At 425 min following ischemic infarct the peak peri-stimulus time response had decreased to 30plusmn11% (electrodes placed 1.5 mm from the infarct core) of the activity before the ischemic onset. The mean response latency increased from 30.1plusmn4.5 ms (before infarct) to 40.6plusmn8.5 ms (at 425 min). This dynamic view of neuroplasticity may eventually assist in optimizing acute stroke therapies and optimize functional recovery further
机译:据信神经塑性在中风后在功能恢复中发挥关键作用。可以通过例如通过例如在细胞水平处监测神经塑性效果。神经递质评估,但这些研究需要牺牲动物。 FMRI可用于评估功能性神经元性能,但空间和时间分辨率远离单个细胞水平。目的是建立一种有效的方法,用于在中风之前,期间和之后的单一和多单元电生理学功能进行短期分析。我们用16-CH阵列在初级电机皮质(100毫米线直径)中用16-CH阵列进行了一只大鼠,以监测皮质活动。在对侧前肢的尺骨神经周围植入双极袖带电极,以提供对感觉电机系统的受控电气刺激。通过在皮质表面处的光敏染料(玫瑰瓣,1.3mg / 100mg体重)轻度激活3mm直径的缺血性梗塞。在皮质缺血性梗死术之前,期间和之后记录了响应外围电刺激的M1活性。在缺血性梗死后425分钟,峰Peri刺激时间响应减少到缺血性发作前的活动的30plumn11%响应降至30plumn11%(从Infarct核心放置1.5mm)。平均响应延迟从30.1plusmn4.5 ms(infarct之前)增加到40.6plusmn8.5 ms(425分钟)。这种神经塑性的动态视图最终可以帮助优化急性卒中疗法并进一步优化功能恢复

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