Nerve injury reduces responses of hypoglossal motoneurones to baseline and chemoreceptor-modulated inspiratory drive in the adult rat
Nerve injury reduces responses of hypoglossal motoneurones to baseline and chemoreceptor-modulated inspiratory drive in the adult rat
复制标题
DOI：
10.1113/jphysiol.2003.059972
复制
发表时间：
2004-06-15
影响因子：
5.5
通讯作者：
Moreno-López, B
中科院分区：
文献类型：
--
作者：
González-Forero, D;Portillo, F;Moreno-López, B
周围神经病变对运动神经元膜和突触特性的影响已被广泛研究。然而，关于这些改变最终如何影响生理传入驱动下的放电活动和运动输出的信息很少。本研究的目的是评估舌下神经压迫对舌下运动神经元（HMN）放电的影响，以响应基础吸气传入驱动及其二氧化碳的化学感觉调节。通过记录XIIth神经刺激引起的复合肌肉动作电位来评估病变的演变，该动作电位在挤压时消失，然后在病变后第2 - 4周逐渐恢复到控制值。损伤后7天，损伤部位近端神经和细胞核的基础呼吸活动分别减少51.6%和35.8%。单个单位的反周期潜伏期因损伤而延长，并且通常需要异常高的刺激强度才能引起反周期峰值。同样，在化学感受器驱动通过改变潮汐末二氧化碳而变化的条件下，单一放电的吸气调节减少了60%以上。虽然在第十二神经损伤后，一般的招募方案得以保留，但我们注意到低阈值单位的比例增加，在整个生理范围内的招募增益减少。舌下核突触素免疫组化染色显示，神经损伤后突触素显著减少。肌肉再神经支配恢复形态和功能改变。因此，我们在此报告，神经损伤引起的改变，在基础活动和HMNs放电调制，同时传入输入的损失。然而，我们认为，其他报道的膜兴奋性的增加，以及低阈值单位的比例，可能有助于保持最小的电活动，防止变性和促进轴突再生。
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 CO2. 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 CO2 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.