MOTONEURON SURVIVAL IS NOT AFFECTED BY THE PROXIMO-DISTAL LEVEL OF AXOTOMY BUT BY THE POSSIBILITY OF REGENERATING AXONS TO GAIN ACCESS TO THE DISTAL NERVE STUMP

The aim of this study was to examine whether axotomy-induced motoneuro n death in adult mammals differ: (1) with the distance between the sit e of injury and the nerve cell body, and (2) if contact between the tr ansected nerve stumps is established after the injury, compared with c ases where contact is prevented.The hypoglossal nerve of adult rats wa s transected either proximally in the neck (proximal injury) or close to the tongue (distal injury). The nerve stumps were then either defle cted from each other in order to prevent axon regeneration into the di stal nerve stump, or sutured. Three months later, the extent of nerve cell loss was examined bilaterally in cresyl violet-stained sections o f the hypoglossal nucleus. In addition, we examined hypoglossal neuron survival twelve months after a proximal nerve transection with preven ted regeneration. Our results show that there was no significant diffe rence in neuronal survival after a proximal nerve transection compared with a distal one, neither if contact between the nerve stumps was es tablished nor if it was prevented. However, contact between the transe cted nerve stumps increased the likelihood of neuronal survival signif icantly after both proximally and distally located injury compared to nerve injury with prevented regeneration. There was no significant dec rease in nerve cell survival after twelve months with prevented reinne rvation compared with survival after three months. These observations indicate that the extent of axotomy-induced motoneuron death in adult mammals does not correlate with the proximo-distal level of peripheral injury. Furthermore, early contact with the distal stump and/or targe t musculature is a significant factor for the survival of axotomized m otoneurons. However, more than 50% of the original nerve cell populati on survives a considerable time even after permanent disconnection fro m the target. (C) 1994 Wiley-Liss, Inc.