Yu X H, Moret V, Rouiller E M
Institute of Physiology, University of Fribourg, Switzerland.
J Hirnforsch. 1995;36(1):123-33.
After unilateral lesion of the sensorimotor cortex in neonatal rats (postnatal days 2-4), the reorganization of the corticothalamic projection originating from the opposite intact sensorimotor cortex was studied. Three months after the lesion, the anterograde tracer phaseolus vulgaris-leucoagglutinin (PHA-L) was injected in the caudal forelimb area (CFA) of the intact opposite sensorimotor cortex to label the corticothalamic axons, in order to establish their trajectory as well as the distribution of their terminal fields in the thalamus. As previously reported, in addition to the standard ipsilateral corticothalamic projection, lesioned rats were characterized also by the presence of a contralateral corticothalamic projection, reaching the decorticate hemithalamus. There is some controversy in literature whether such bilateral corticothalamic projection is present in normal intact rats. On the basis of counts of axons crossing the midline to innervate the hemithalamus contralateral to the cortical injection, the present study provides evidence that the corticothalamic projection is indeed bilateral in normal rats, although the contralateral projection is sparse. Lesioned rats subjected to a similar small size PHA-L injection in the CFA of the intact opposite cortex showed a significantly increased contralateral corticothalamic projection. The number of labeled axons crossing the midline in the thalamus was, on average, five times higher in lesioned rats than in normal rats. It can be concluded that the contralateral corticothalamic projection from the CFA, observed after neonatal lesion of the opposite sensorimotor cortex, is not a novel projection resulting from the lesion, but rather an enhancement and extension of an existing, minor, projection present in normal rats. The enhancement of the crossing corticothalamic projection in lesioned rats is due to an increase of the number of crossing axons in the thalamus rather than to an increase of the degree of branching of the few axons present in control animals.
在新生大鼠（出生后2 - 4天）单侧损伤感觉运动皮层后，研究了源自对侧完整感觉运动皮层的皮质丘脑投射的重组情况。损伤三个月后，将顺行示踪剂菜豆凝集素（PHA-L）注入对侧完整感觉运动皮层的尾侧前肢区（CFA），以标记皮质丘脑轴突，从而确定其轨迹以及它们在丘脑中终末场的分布。如先前报道的那样，除了标准的同侧皮质丘脑投射外，损伤大鼠的特征还在于存在对侧皮质丘脑投射，该投射到达去皮质半脑。文献中对于正常完整大鼠是否存在这种双侧皮质丘脑投射存在一些争议。基于对穿过中线以支配与皮质注射相对侧半脑的轴突计数，本研究提供了证据表明正常大鼠的皮质丘脑投射确实是双侧的，尽管对侧投射稀疏。在对侧完整皮层的CFA中接受类似小剂量PHA-L注射的损伤大鼠显示对侧皮质丘脑投射显著增加。在丘脑中穿过中线的标记轴突数量，损伤大鼠平均比正常大鼠高五倍。可以得出结论，在对侧感觉运动皮层新生损伤后观察到的来自CFA的对侧皮质丘脑投射，不是损伤产生的新投射，而是正常大鼠中存在的现有少量投射的增强和扩展。损伤大鼠中交叉皮质丘脑投射的增强是由于丘脑中交叉轴突数量的增加，而不是由于对照动物中少量轴突分支程度的增加。
