title: Central drive on Renshaw cells coupled with phrenic motoneurons.
abstract: In anesthetized spontaneously breathing cats (C4-C5 deafferentation), recurrent inhibition of phrenic motoneurons was analyzed by studying either recurrent IPSPs in phrenic motoneurons, or Renshaw cell discharges evoked by C5 phrenic nerve stimulation. Of 90 intracellularly recorded phrenic motoneurons, 7 motoneurons showed evoked recurrent IPSPs with stimulation of C5 phrenic axons subthreshold for eliciting antidromic activation of the motoneuron from which intracellular recording was done. These IPSPs could be reversed by imposed hyperpolarization of the motoneuron, and were of greater amplitude during inspiration than during expiration. Within the phrenic nucleus, interneurons were classified as Renshaw cells if they responded to C5 phrenic axon stimulation with a typical high frequency burst of potentials. Reactivity of these Renshaw cells was related to the respiratory cycle, number of spikes in the burst being greater during inspiration than during expiration. Injection of a nicotinic cholinergic blocker (mecamylamine) decreased responses of Renshaw cells but the respiratory modulation was still present. Some Renshaw cells (18/33) were spontaneously active during inspiration. Their activity was generally maximal during the last third of inspiration. Since: spontaneous activity of Renshaw cells is related to the respiratory drive; persists after C7 spinal transection and after mecamylamine poisoning of the axonal recurrent pathway; and might appear before sustained phrenic activity, the assumption of a central respiratory drive impinging on the Renshaw cells has to be retained.
mesh_terms: D000818:Animals; D002415:Cats; D002490:Central Nervous System / Q000502:physiology*; D007395:Interneurons / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D009433:Neural Inhibition; D010791:Phrenic Nerve / Q000166:cytology / Q000502:physiology*; D012143:Respiratory Physiological Phenomena; D013116:Spinal Cord / Q000502:physiology*