Sensory-motor deficit and recovery from thrombotic infarction of the vibrissal barrel-field cortex

The present studies were undertaken to examine: (1) whether thrombotic infarction of the vibrissal cortical barrel-fields of the primary somatosensory cortex would produce behavioral consequences reflecting a sensory-motor deficit; and (2) whether there was any recovery of function up to two months after infarction. Specifically, in two different learning tasks requiring sensory-motor integration, rats were trained to perform a motor response consequent to the detection of vibrissal cues derived from either active exploration or from passive detection of vibrissal deflection. Once training was complete, unilateral, bilateral or sham-infarction restricted to the region of the primary somatosensory cortex was produced by a non-invasive photochemical technique, which induces platelet-activated vascular occlusion combined with blood-brain barrier changes and subsequent cell death. The results demonstrated that, regardless of the active or passive sensory characteristics of the task, unilateral and bilateral infarction resulted in a reliable performance deficit, which was not present in sham-operated control animals. Thus, the infarct disrupted the ability to integrate passively received or actively acquired vibrissal sensory information with a previously associated motor response. However, unlike the bilaterally infarcted animals, who displayed no recovery of performance level throughout the postinfarction testing sessions, the unilaterally infarcted animals exhibited a gradual improvement in performance beginning in the second or third week postinfarction and recovering to within 10–20% of preinfarction levels between postinfarction days 46–61. The similarity of the temporal pattern of behavioral recovery in the unilateral groups, despite large differences in the sensory-motor demands of the two tasks, may reflect several common underlying mechanisms of recovery. Since similar sensory-motor behavioral deficits and recovery have been described with human stroke, the present model incorporates many of the pathophysiological and behavioral properties present in the clinical situation and may be useful for future investigation of therapeutic intervention.

进行本研究是为了检验：（1）初级躯体感觉皮层的触须皮质桶状区域的血栓性梗死是否会产生反映感觉 - 运动缺陷的行为后果；（2）梗死发生后长达两个月是否有任何功能恢复。具体而言，在两项需要感觉 - 运动整合的不同学习任务中，训练大鼠在检测到由主动探索或被动检测触须偏转所产生的触须线索后做出运动反应。一旦训练完成，通过一种非侵入性光化学技术在初级躯体感觉皮层区域制造单侧、双侧或假梗死，该技术诱导血小板激活的血管闭塞，同时伴有血脑屏障改变和随后的细胞死亡。结果表明，无论任务的主动或被动感觉特性如何，单侧和双侧梗死都会导致可靠的行为表现缺陷，而在假手术对照动物中则不存在这种情况。因此，梗死破坏了将被动接收或主动获取的触须感觉信息与先前相关的运动反应相结合的能力。然而，与双侧梗死的动物不同，双侧梗死的动物在整个梗死后测试期间行为表现水平没有恢复，单侧梗死的动物在梗死后第二或第三周开始行为表现逐渐改善，并在梗死后第46 - 61天恢复到梗死前水平的10 - 20%以内。尽管两项任务的感觉 - 运动要求存在很大差异，但单侧组行为恢复的时间模式相似，这可能反映了几种常见的恢复潜在机制。由于人类中风也描述了类似的感觉 - 运动行为缺陷和恢复，本模型包含了临床情况中存在的许多病理生理和行为特性，可能对未来治疗干预的研究有用。