MOTONEURON SURVIVAL AFTER NEONATAL PERONEAL NERVE INJURY IN THE RAT -EVIDENCE FOR THE SPARING EFFECT OF RECIPROCAL INHIBITION

Citation
Hj. Waters et al., MOTONEURON SURVIVAL AFTER NEONATAL PERONEAL NERVE INJURY IN THE RAT -EVIDENCE FOR THE SPARING EFFECT OF RECIPROCAL INHIBITION, Experimental neurology, 152(1), 1998, pp. 95-100
Citations number
36
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
152
Issue
1
Year of publication
1998
Pages
95 - 100
Database
ISI
SICI code
0014-4886(1998)152:1<95:MSANPN>2.0.ZU;2-G
Abstract
Sciatic nerve crush at birth results in the death of most of the moton eurons in the sciatic motor pool. It has been proposed that these cell s die through excessive activation which can be explained partly by an increased susceptibility to NMDA. However, it is also possible that d ecreased inhibitory mechanisms resulting from nerve injury may contrib ute to overactivation of the motoneurons. In this study we compared th e survival of motoneurons innervating two muscles in the peroneal moto r pool, tibialis anterior and extensor digitorum longus, after either sciatic or common peroneal nerve crush. These two procedures both axot omize the motoneurons but differ in their effects on afferent input. S ciatic nerve crush severely reduces the afferent input from the antago nist muscles innervated via the tibial nerve, whereas common peroneal nerve crush preserves them. Using retrograde labeling with horseradish peroxidase, we found that almost twice as many motoneurons survived c ommon peroneal nerve crush than sciatic nerve crush and that muscle we ight showed a corresponding significant improvement. A control experim ent excluded the possible involvement of increased stretch of the musc les as a result of common peroneal nerve crush alone as an explanation for the improvement. We therefore suggest that the increased survival of motoneurons after peroneal nerve crush was due to the preservation of their reciprocal inhibitory input. However, since even with this i mprovement the majority of motoneurons still died, loss of reciprocal inhibition probably does not play a major role in the death of motoneu rons induced by overactivation. (C) 1998 Academic Press.