Departamento de Fisiología, Universidad de Sevilla, Avda. Reina Mercedes, 6, 41012, Seville, Spain.
Brain Struct Funct. 2019 Nov;224(8):2717-2731. doi: 10.1007/s00429-019-01929-2. Epub 2019 Aug 2.
Medial rectus motoneurons are innervated by two main pontine inputs. The specific function of each of these two inputs remains to be fully understood. Indeed, selective partial deafferentation of medial rectus motoneurons, performed by the lesion of either the vestibular or the abducens input, initially induces similar changes in motoneuronal discharge. However, at longer time periods, the responses to both lesions are dissimilar. Alterations on eye movements and motoneuronal discharge induced by vestibular input transection recover completely 2 months post-lesion, whereas changes induced by abducens internuclear lesion are more drastic and permanent. Functional recovery could be due to some kind of plastic process, such as reactive synaptogenesis, developed by the remaining intact input, which would occupy the vacant synaptic spaces left after lesion. Herein, by means of confocal microscopy, immunocytochemistry and retrograde labeling, we attempt to elucidate the possible plastic processes that take place after partial deafferentation of medial rectus motoneuron. 48 h post-injury, both vestibular and abducens internuclear lesions produced a reduced synaptic coverage on these motoneurons. However, 96 h after vestibular lesion, there was a partial recovery in the number of synaptic contacts. This suggests that there was reactive synaptogenesis. This recovery was preceded by an increase in somatic neurotrophin content, suggesting a role of these molecules in presynaptic axonal sprouting. The rise in synaptic coverage might be due to terminal sprouting performed by the remaining main input, i.e., abducens internuclear neurons. The present results may improve the understanding of this apparently redundant input system.
内侧直肌运动神经元接受两个主要的脑桥传入。这两个输入的具体功能仍有待完全理解。事实上,内侧直肌运动神经元的选择性部分去传入,通过前庭或展神经输入的损伤来完成,最初会引起运动神经元放电的相似变化。然而,在更长的时间内,这两种损伤的反应是不同的。前庭传入切断后引起的眼动和运动神经元放电的改变在损伤后 2 个月完全恢复,而展神经核间损伤引起的改变则更为剧烈和持久。功能恢复可能是由于某种可塑性过程,例如剩余的完整输入所发展的反应性突触形成,它会占据损伤后留下的空闲突触空间。在此,通过共聚焦显微镜、免疫细胞化学和逆行标记,我们试图阐明内侧直肌运动神经元部分去传入后可能发生的可塑性过程。损伤后 48 小时,前庭和展神经核间损伤均导致这些运动神经元的突触覆盖减少。然而,前庭损伤后 96 小时,突触接触数部分恢复。这表明存在反应性突触形成。这种恢复之前是体细胞神经生长因子含量的增加,表明这些分子在前突触轴突发芽中起作用。突触覆盖的增加可能是由于剩余的主要输入,即展神经核间神经元,进行了末端发芽。这些结果可能有助于更好地理解这个明显冗余的输入系统。