QUANTITATIVE ASSESSMENT OF THE EFFECT OF CHRONIC PHRENICOTOMY ON THE INDUCTION OF THE CROSSED PHRENIC PHENOMENON

The present study was carried out to determine if chronic peripheral p hrenicotomy has a functional influence on the plasticity that is norma lly demonstrated by phrenic motoneurons in the spinal cord following s pinal cord injury. Young adult female Sprague-Dawley rats were divided into an experimental and a control group. Left intrathoracic phrenico tomies were carried out at 1, 2, 3, and 4 weeks prior to induction of the crossed phrenic phenomenon and crossed phrenic nerve activity reco rding in the experimental group. Control animals were not subjected to chronic phrenicotomy. In each animal the crossed phrenic phenomenon w as induced by left C2 spinal cord hemisection and turning off the vent ilator. The reflex-induced activity in the phrenic nerve ipsilaterd to hemisection is defined as ''crossed phrenic nerve activity.'' All ani mals were subjected to spinal cord hemisection 24 h before crossed phr enic nerve activity recording. The results showed that there is a tran sient but statistically significant depression of crossed phrenic nerv e activity at 2 weeks postphrenicotomy and a recovery to the normal ac tivity level at 4 weeks postphrenicotomy. One control experiment was c arried out to assess the effects of phrenicotomy on respiratory activi ty that is normally present in the phrenic nerve (i.e., not reflex- in duced). This ''primary respiratory nerve activity'' is different from crossed phrenic nerve activity in that the phrenic motoneurons are dri ven by different bulbospinal respiratory pathways. The results indicat ed a marked decrease in primary respiratory nerve activity at 1 week a fter phrenicotomy with no significant recovery by the 4th week after p hrenicotomy. Two other control experiments were performed to rule out the possibility that the alteration in crossed phrenic nerve activity in the experimental animals is the result of (1) conduction changes in the transected phrenic nerve fibers or (2) reinnervation of the diaph ragm by the transected phrenic nerves. From the results, we conclude t hat the depression of crossed phrenic nerve activity at 2 weeks postph renicotomy is most likely due to transient changes in the phrenic nucl eus that prevent the expression of the crossed phrenic nerve activity. The conditions which cause a depression of the reflex activity at 2 w eeks are no longer present at 4 weeks postphrenicotomy. The mechanism for the depression of reflex activity at 2 weeks is as yet unknown. (C ) 1994 Academic Press, Inc.