Isa Tadashi, Kinoshita Masaharu, Nishimura Yukio
Department of Developmental Physiology, National Institute for Physiological Sciences , Okazaki , Japan ; Department of Life Sciences, Graduate University for Advanced Studies (SOKENDAI) , Hayama , Japan.
Front Neurol. 2013 Nov 19;4:191. doi: 10.3389/fneur.2013.00191.
Evolutionally, development of the direct connection from the motor cortex to spinal motoneurons [corticomotoneuronal (CM) pathway] parallels the ability of hand dexterity. Damage to the corticofugal fibers in higher primates resulted in deficit of fractionated digit movements. Based on such observations, it was generally believed that the CM pathway plays a critical role in the control of hand dexterity. On the other hand, a number of "phylogenetically older" indirect pathways from the motor cortex to motoneurons still exist in primates. The indirect pathways are mediated by intercalated neurons such as segmental interneurons (sINs), propriospinal neurons (PNs) reticulospinal neurons (RSNs), or rubrospinal neurons (RuSNs). However, their contribution to hand dexterity remains elusive. Lesion of the brainstem pyramid sparing the transmission through the RuSNs and RSNs, resulted in permanent deficit of fractionated digit movements in macaque monkeys. On the other hand, in our recent study, after lesion of the dorsolateral funiculus (DLF) at the C5 segment, which removed the lateral corticospinal tract (l-CST) including the CM pathway and the transmission through sINs and RuSNs but spared the processing through the PNs and RSNs, fractionated digit movements recovered within several weeks. These results suggest that the PNs can be involved in the recovery of fractionated digit movements, but the RSNs and RuSNs have less capacity in this regard. However, on closer inspection, it was found that the activation pattern of hand and arm muscles considerably changed after the C5 lesion, suggesting limitation of PNs for the compensation of hand dexterity. Altogether, it is suggested that PNs, RSNs RuSNs, and the CM pathway (plus sINs) make a different contribution to the hand dexterity and appearance of motor deficit of the hand dexterity caused by damage to the corticofugal fibers and potential of recovery varies depending on the rostrocaudal level of the lesion.
从进化角度来看,运动皮层与脊髓运动神经元之间直接连接[皮质脊髓运动神经元(CM)通路]的发育与手部灵活性的发展并行。高等灵长类动物中皮质离心纤维受损会导致手指精细运动功能障碍。基于这些观察结果,人们普遍认为CM通路在手部灵活性控制中起关键作用。另一方面,灵长类动物中仍存在许多从运动皮层到运动神经元的“系统发生上较古老”的间接通路。这些间接通路由中间神经元介导,如节段性中间神经元(sINs)、脊髓 propriospinal神经元(PNs)、网状脊髓神经元(RSNs)或红核脊髓神经元(RuSNs)。然而,它们对手部灵活性的贡献仍不明确。保留通过红核脊髓神经元和网状脊髓神经元的传导而损伤脑干锥体,导致猕猴出现永久性手指精细运动功能障碍。另一方面,在我们最近的研究中,在C5节段损伤背外侧索(DLF)后,去除了包括CM通路以及通过sINs和红核脊髓神经元的传导,但保留了通过PNs和RSNs的传导,手指精细运动在几周内恢复。这些结果表明PNs可参与手指精细运动的恢复,但RSNs和红核脊髓神经元在这方面的能力较弱。然而,仔细观察发现,C5损伤后手部和手臂肌肉的激活模式发生了很大变化,这表明PNs在补偿手部灵活性方面存在局限性。总之,提示PNs、RSNs、红核脊髓神经元以及CM通路(加上sINs)对手部灵活性以及皮质离心纤维损伤导致的手部灵活性运动功能障碍的出现有不同贡献,恢复潜力因损伤的头尾水平而异。