Anoxic persistence of lumbar respiratory bursts and block of lumbar locomotion in newborn rat brainstem-spinal cords

The tolerance of breathing in neonates to oxygen depletion is reflected by persistence of inspiratory-related motor output during sustained anoxia in newborn rat brainstem preparations. It is not known whether lumbar motor networks innervating expiratory abdominal muscles are, in contrast, inhibited by anoxia similar to locomotor networks in neonatal mouse lumbar cords. To test this, we recorded inspiratory-related cervical/hypoglossal plus pre/postinspiratory lumbar/facial nerve activities and, sometimes simultaneously, locomotor rhythms in newborn rat brainstem–spinal cords. Chemical anoxia slowed 1 : 1-coupled cervical and lumbar respiratory rhythms and induced cervical burst doublets associated with depressed preinspiratory and augmented postinspiratory lumbar activities. Similarly, anoxia evoked repetitive hypoglossal bursts and shifted facial activity toward augmented postinspiratory bursting in medullas without spinal cord. Selective lumbar anoxia augmented pre/postinspiratory lumbar bursting without slowing the rhythm. This suggests a medullary origin of both anoxic inspiratory double bursts and preinspiratory depression, but a mixed medullary/lumbar origin of boosted postinspiratory lumbar activity. Lumbar respiratory rhythm is likely to be generated by the parafacial respiratory group expiratory centre as indicated by lack of normoxic and anoxic bursting following brainstem transection between the facial motonucleus and the more caudal pre-B¨otzinger complex inspiratory centre. Opposed to sustained respiratory activities, anoxia reversibly abolished non-rhythmic spinal discharges and electrically or chemically evoked lumbar locomotor activities, followed by pronounced postanoxic spinal hyperexcitability. We hypothesize that (i) the anoxia tolerance of neonatal breathing includes pFRG-driven lumbar expiratory networks, (ii) the anoxic respiratory pattern transformation is due to disturbed inspiratory–expiratory centre interactions, and (iii) postanoxic lumbar hyperexcitability contributes to spasticity in cerebral palsy.