Jankowska E, Cabaj A, Pettersson L-G
Department of Physiology, Göteborg University, 405 30 Göteborg, Sweden.
J Neurosci. 2005 Aug 10;25(32):7401-5. doi: 10.1523/JNEUROSCI.1838-05.2005.
We have shown previously that ipsilateral pyramidal tract (PT) neurons facilitate the actions of reticulospinal neurons on feline motoneurons (Edgley et al., 2004), which indicates that they might assist the recovery of motor functions after injuries of contralateral corticospinal neurons. Nevertheless, stimulation of ipsilateral PT fibers alone only rarely evoked any synaptic actions in motoneurons. The aim of this study was to investigate possible ways of enhancing such actions and of inducing more effective excitation and inhibition of motoneurons. The effects of stimulation of the ipsilateral PT were investigated after eliminating the spinal actions of contralateral PT fibers by hemisecting the spinal cord at a low thoracic level and were estimated from intracellular records from hindlimb motoneurons. Two measures were used to enhance PT actions. The first was to increase the probability of activation of reticulospinal neurons by mutual facilitation of actions of ipsilateral and contralateral PT neurons. The second was to enhance synaptic transmission between PT neurons and reticulospinal neurons, and in pathways between the reticulospinal neurons and motoneurons via commissural interneurons, by systemic application of a K+ channel blocker, 4-aminopyridine (4-AP). The results show that under favorable conditions, ipsilateral PT neurons may induce EPSPs and IPSPs in hindlimb motoneurons, or even action potentials, via the reticulospinal pathway. This study strengthens previous conclusions that ipsilateral PT neurons can potentially replace, at least to some extent, the actions of injured contralateral PT neurons. It also suggests that 4-AP might improve the progress of the recovery.
我们之前已经表明，同侧锥体束（PT）神经元可促进网状脊髓神经元对猫运动神经元的作用（埃奇利等人，2004年），这表明它们可能有助于对侧皮质脊髓神经元损伤后运动功能的恢复。然而，仅刺激同侧PT纤维很少能在运动神经元中诱发任何突触作用。本研究的目的是探讨增强此类作用以及诱导对运动神经元更有效兴奋和抑制的可能方法。在胸段低位水平对脊髓进行半横切以消除对侧PT纤维的脊髓作用后，研究了同侧PT刺激的效果，并根据后肢运动神经元的细胞内记录进行评估。采用了两种措施来增强PT的作用。第一种是通过同侧和对侧PT神经元作用的相互促进来增加网状脊髓神经元激活的概率。第二种是通过全身应用钾通道阻滞剂4-氨基吡啶（4-AP）来增强PT神经元与网状脊髓神经元之间以及通过连合中间神经元在网状脊髓神经元与运动神经元之间的突触传递。结果表明，在有利条件下，同侧PT神经元可通过网状脊髓途径在后肢运动神经元中诱发兴奋性突触后电位（EPSP）和抑制性突触后电位（IPSP），甚至动作电位。本研究强化了先前的结论，即同侧PT神经元至少在一定程度上可以潜在地替代受损对侧PT神经元的作用。它还表明4-AP可能会改善恢复进程。
