Department of Psychiatry, Brain Research Centre, University of British Columbia, Vancouver, BC, Canada.
Stroke. 2013 Aug;44(8):2300-6. doi: 10.1161/STROKEAHA.113.001272. Epub 2013 Jun 6.
Recovery from stroke is hypothesized to involve the reorganization of surviving cortical areas. To study the functional organization of sensorimotor cortex at multiple time points before and after stroke, we performed longitudinal light-based motor mapping of transgenic mice expressing light-sensitive channelrhodopsin-2 in layer 5 cortical neurons.
Pulses of light stimulation were targeted to an array of cortical points, whereas evoked forelimb motor activity was recorded using noninvasive motion sensors. Intrinsic optical signal imaging produced maps of the forelimb somatosensory cortex. The resulting motor and sensory maps were repeatedly generated for weeks before and after small (0.2 mm3) photothrombotic infarcts were targeted to forelimb motor or sensory cortex.
Infarcts targeted to forelimb sensory or motor areas caused decreased motor output in the infarct area and spatial displacement of sensory and motor maps. Strokes in sensory cortex caused the sensory map to move into motor cortex, which adopted a more diffuse structure. Stroke in motor cortex caused a compensatory increase in peri-infarct motor output, but did not affect the position or excitability of sensory maps.
After stroke in motor cortex, decreased motor output from the infarcted area was offset by peri-infarct excitability. Sensory stroke caused a new sensory map to form in motor cortex, which maintained its center position, despite becoming more diffuse. These data suggest that surviving regions of cortex are able to assume functions from stroke-damaged areas, although this may come at the cost of alterations in map structure.
中风后的恢复被假设涉及存活的皮质区域的重组。为了在中风前后的多个时间点研究感觉运动皮质的功能组织，我们对表达光敏感通道视紫红质-2 的转基因小鼠进行了基于光的运动映射的纵向研究，该蛋白在皮质 5 层神经元中表达。
将光刺激脉冲靶向于皮质点阵列，而诱发出的前肢运动活动则使用非侵入性运动传感器进行记录。固有光学信号成像产生了前肢体感皮质的图谱。在将小（0.2mm3）光血栓形成梗塞靶向于前肢运动或感觉皮质之前和之后的数周内，反复生成这些运动和感觉图谱。
靶向于前肢感觉或运动区域的梗塞导致梗塞区域的运动输出减少，并且感觉和运动图谱的空间移位。感觉皮质中的中风导致感觉图谱移动到运动皮质，后者具有更弥散的结构。运动皮质中的中风导致梗塞周围运动输出的代偿性增加，但不影响感觉图谱的位置或兴奋性。
在运动皮质中风后，梗塞区域的运动输出减少被梗塞周围的兴奋性所抵消。感觉中风导致新的感觉图谱在前运动皮质中形成，尽管变得更加弥散，但仍保持其中心位置。这些数据表明，尽管可能会以图谱结构的改变为代价，但皮质的存活区域能够承担受损区域的功能。
