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Following brain damage, especially in juvenile animals, large-scale reorganization is known to occur in the remaining brain structures to compensate for functional deficits. In rats with neonatal hemidecortication, corticospinal fibers originating from the undamaged side of the sensorimotor cortex issue collateral sprouts to the ipsilateral spinal gray matter that mediate cortical excitation to ipsilateral forelimb motoneurons and compensate for the deficit in forelimb movements. The present study was designed to investigate the origins of the ipsilateral corticospinal projection in neonatally hemidecorticated rats. Corticospinal neurons (CSNs) were labeled in adults by injecting retrograde neural tracers, cholera toxin subunit B with different fluorescent probes, into either side of the cervical spinal gray matter. In the undamaged cortex, double-labeled neurons were rarely found. CSNs with contralateral projections (contra-CSNs) and those with ipsilateral projections (ipsi-CSNs) were distributed both in the rostral forelimb motor area (RFA) and the caudal forelimb motor area (CFA). However, there was a difference in the distributions of the ipsi-CSNs between the two forelimb areas. Whereas the distribution of the ipsi-CSNs largely overlapped with that of the contra-CSNs in the RFA, the ipsi-CSNs tended to be segregated from the contra-CSNs in the CFA. The results suggested that the RFA and the CFA contribute to the compensatory process in different ways.  相似文献   

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实验旨在运用生物素标记葡聚糖胺神经束路示踪标记神经干细胞移植治疗脊髓损伤后皮质脊髓束的再生和神经的重新支配状况,结果表明神经干细胞移植治疗胸10脊髓横断损伤大鼠运动功能评分在横断损伤3周后逐渐升高。治疗后12周有部分生物素标记葡聚糖胺阳性标记的皮质脊髓束再生通过脊髓横断损伤部位,电镜检查发现再生的生物素标记葡聚糖胺阳性标记的神经终末与损伤远端神经元形成新的突触联系。说明生物素标记葡聚糖胺神经束路示踪能有效提供脊髓损伤后神经恢复的解剖形态学依据。  相似文献   

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对皮质脊髓束的可视化示踪研究主要集中在啮齿目动物鼠类,与人类脊髓结构差异较大,本文运用数字减影血管造影技术对山羊脊髓节段供血动脉进行栓塞,制备缺血性脊髓损伤动物模型,将生物素化葡聚糖胺注入缺血性脊髓损伤动物的皮质运动功能区。显示山羊皮质脊髓束起源于大脑皮质运动功能区,经锥体交叉后走行于对侧脊髓后角前方的侧索内,从头端至尾端皮质脊髓束阳性纤维数目逐渐减少。由此认为数字减影血管造影技术可制备山羊缺血性脊髓损伤模型,以生物素化葡聚糖胺显示山羊皮质脊髓束在脊髓内的走行特点与人类有相似之处,说明生物素化葡聚糖胺是皮质脊髓束可视化研究的理想示踪剂。  相似文献   

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Unilateral damage to cortical areas in the frontal cortex produces sensorimotor deficits on the side contralateral to the lesion. Although there are anecdotal reports of bilateral deficits after stroke in humans and in experimental animals, little is known of the effects of unilateral lesions on the same side of the body. The objective of the present study was to make a systematic examination of the motor skills of the ipsilateral forelimb after frontal cortex lesions to either the motor cortex by devascularization of the surface blood vessels (pial stroke), or to the lateral cortex by electrocoagulation of the distal branches of the middle cerebral artery (MCA stroke). Plastic processes in the intact hemisphere were documented using Golgi-Cox dendritic analysis and by intracortical microstimulation analysis. Although tests of reflexive responses in forelimb placing identified a contralateral motor impairment following both cortical lesions, quantitative and qualitative measures of skilled reaching identified a severe ipsilateral impairment from which recovery was substantial but incomplete. Golgi-impregnated pyramidal cells in the forelimb area showed an increase in dendritic length and branching. Electrophysiological mapping showed normal size forelimb representations in the lesioned rats relative to control animals. The finding of an enduring ipsilateral impairment in skilled movement is consistent with a large but more anecdotal literature in rats, nonhuman primates and humans, and suggests that plastic changes in the intact hemisphere are related to that hemisphere's contribution to skilled movement.  相似文献   

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