Nerve injury reduces responses of hypoglossal motoneurones to baseline and chemoreceptor-modulated inspiratory drive in the adult rat.
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.
González-Forero
David
D
Area de Fisiologia, Facultad de Medicina, Universidad de Cádiz, Plaza Falla, 9, 11003 Cadiz, Spain.
Portillo
Federico
F
Sunico
Carmen R
CR
Moreno-López
Bernardo
B
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D019771:Axotomy; D002245:Carbon Dioxide / Q000494:pharmacology; D002454:Cell Differentiation; D002628:Chemoreceptor Cells / Q000502:physiology*; D004576:Electromyography; D007002:Hypoglossal Nerve / Q000166:cytology; D061228:Hypoglossal Nerve Injuries; D007150:Immunohistochemistry; D008297:Male; D009046:Motor Neurons / Q000502:physiology*; D009409:Nerve Crush; D009469:Neuromuscular Junction / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D015656:Respiratory Mechanics / Q000502:physiology*; D016708:Synaptophysin / Q000502:physiology
D016708:Synaptophysin; D002245:Carbon Dioxide