González-Forero David, Portillo Federico, Sunico Carmen R, Moreno-López Bernardo
Area de Fisiologia, Facultad de Medicina, Universidad de Cádiz, Plaza Falla, 9, 11003 Cadiz, Spain.
J Physiol. 2004 Jun 15;557(Pt 3):991-1011. doi: 10.1113/jphysiol.2003.059972. Epub 2004 Apr 16.
The effects of peripheral nerve lesions on the membrane and synaptic properties of motoneurones have been extensively studied. However, minimal information exists about how these alterations finally influence discharge activity and motor output under physiological afferent drive. The aim of this work was to evaluate the effect of hypoglossal (XIIth) nerve crushing on hypoglossal motoneurone (HMN) discharge in response to the basal inspiratory afferent drive and its chemosensory modulation by CO(2). The evolution of the lesion was assessed by recording the compound muscle action potential evoked by XIIth nerve stimulation, which was lost on crushing and then recovered gradually to control values from the second to fourth weeks post-lesion. Basal inspiratory activities recorded 7 days post-injury in the nerve proximal to the lesion site, and in the nucleus, were reduced by 51.6% and 35.8%, respectively. Single unit antidromic latencies were lengthened by lesion, and unusually high stimulation intensities were frequently required to elicit antidromic spikes. Likewise, inspiratory modulation of unitary discharge under conditions in which chemoreceptor drive was varied by altering end-tidal CO(2) was reduced by more than 60%. Although the general recruitment scheme was preserved after XIIth nerve lesion, we noticed an increased proportion of low-threshold units and a reduced recruitment gain across the physiological range. Immunohistochemical staining of synaptophysin in the hypoglossal nuclei revealed significant reductions of this synaptic marker after nerve injury. Morphological and functional alterations recovered with muscle re-innervation. Thus, we report here that nerve lesion induced changes in the basal activity and discharge modulation of HMNs, concurrent with the loss of afferent inputs. Nevertheless, we suggest that an increase in membrane excitability, reported by others, and in the proportion of low-threshold units, could serve to preserve minimal electrical activity, prevent degeneration and favour axonal regeneration.
外周神经损伤对运动神经元膜特性和突触特性的影响已得到广泛研究。然而，关于这些改变最终如何在生理传入驱动下影响放电活动和运动输出的信息却很少。本研究的目的是评估舌下神经（第 XII 对脑神经）挤压伤对舌下运动神经元（HMN）在基础吸气传入驱动下的放电以及 CO₂ 对其化学感受性调制的影响。通过记录第 XII 对脑神经刺激诱发的复合肌肉动作电位来评估损伤的进展，该电位在挤压伤时消失，然后在损伤后第二至第四周逐渐恢复到对照值。损伤后 7 天在损伤部位近端神经以及核内记录的基础吸气活动分别降低了 51.6%和 35.8%。损伤使单单位逆向潜伏期延长，并且经常需要异常高的刺激强度才能诱发逆向峰电位。同样，在通过改变呼气末 CO₂ 来改变化学感受器驱动的条件下，单位放电的吸气调制降低了 60%以上。尽管第 XII 对脑神经损伤后总体募集模式得以保留，但我们注意到低阈值单位的比例增加，并且在整个生理范围内募集增益降低。舌下神经核中突触素的免疫组织化学染色显示神经损伤后该突触标记物显著减少。形态学和功能改变随着肌肉再支配而恢复。因此，我们在此报告神经损伤引起了 HMN 的基础活动和放电调制的变化，同时伴有传入输入的丧失。然而，我们认为其他人报道的膜兴奋性增加以及低阈值单位比例的增加可能有助于维持最低限度的电活动、防止退变并有利于轴突再生。
