Basis for late expiratory spinal inhibition of phrenic nerve discharge.
The relationship between spinal inhibition of phrenic nerve activity and thoratic expiratory motoneuronal discharge was studied in chloralose-anesthetized and unanesthetized decerebrate cats.  The amplitude of the phrenic nerve response elicited by singleshocks applied to descending tracts in the second cervical spinal segment progressively fell during the late expiratory phase of the central respiratory cycle.  The depression resulted, at least in part, from active spinal inhibition since the spina-to-phrenic evoked response was smaller in late expiration than after C'1 spinal transection.  Inhibition of the spinal-to-phrenic evoked was time-locked to the spontaneousburst of activity recorded from the eigth internal intercostal nerve.  The degree of inhibition of the spinal-to-phenic evoked discharge was directly related to theamplitude of spontaneously occurring internal intercostal nerve activity.  A similiarrelationship was observed when internal intercostal nerve activity and spinal inhibitionof phrenic discharge were evoked by stimulation of the superior laryngeal nerve.  It is concluded htat late expiratory spinal inhibition of phrenic discharge was dependent on those neural events responsible for the activation of thoracic expiratory motoneurons.
D000818:Animals; D002415:Cats; D002541:Cerebral Decortication; D002574:Cervical Vertebrae; D002818:Cordotomy; D004558:Electric Stimulation; D005071:Evoked Potentials; D007823:Laryngeal Nerves / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology; D009433:Neural Inhibition; D010424:Pentobarbital / Q000494:pharmacology; D010791:Phrenic Nerve / Q000502:physiology*; D012119:Respiration; D013116:Spinal Cord / Q000502:physiology*; D013900:Thoracic Nerves / Q000502:physiology*
D010424:Pentobarbital