Glutamate receptors in spinal motoneurons after sciatic nerve transection.

Severing the axon of a neuron triggers profound changes in its soma, beginning within a few days and becoming maximal within a few weeks. Unravelling these changes bears directly on our understanding of degeneration and regeneration after injury. Classically described chromatolysis arises from reorganization of rough endoplasmic reticulum, associated with biosynthetic changes in response to injury. Since motoneurons, in contrast with other central neurons, are able to regenerate their axons, their response to axotomy is of special interest. For successful regeneration, a neuron must shift its cellular machinery from "operational" (e.g., integration of synaptic currents, conduction of action potentials, release of transmitter) to "regenerative" (e.g., repair of membrane and axoplasm, remyelination, growth cone guidance). Motoneurons become unresponsive to synaptic input after axotomy, and the conduction velocity of the proximal stump is reduced. The loss of synaptic contacts on to axotomized neurons has been suggested to underlie this lost responsiveness. Here, we demonstrate rapid, selective and dramatic changes in immunostaining for ionotropic glutamate receptors in axotomized motoneurons and in supporting cells, suggesting that altered expression of glutamate receptors underlies the changed reflex responsivity.