GLUTAMATE RECEPTORS IN SPINAL MOTONEURONS AFTER SCIATIC-NERVE TRANSECTION

Severing the axon of a neuron triggers profound changes in its soma, b eginning within a few days and becoming maximal within a few weeks. Un ravelling these changes bears directly on our understanding of degener ation and regeneration after injury. Classically described chromatolys is arises from reorganization of rough endoplasmic reticulum, associat ed 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 successfu l regeneration, a neuron must shift its cellular machinery from ''oper ational'' (e.g., integration of synaptic currents, conduction of actio n potentials, release of transmitter) to ''regenerative'' (e.g., repai r of membrane and axoplasm, remyelination, growth cone guidance). Moto neurons become unresponsive to synaptic input after axotomy, and the c onduction velocity of the proximal stump is reduced.(4,14,17,26) The l oss of synaptic contacts on to axotomized neurons has been suggested t o underlie this lost responsiveness.(2,3,13,23,31) Here, we demonstrat e rapid, selective and dramatic changes in immunostaining for ionotrop ic glutamate receptors in axotomized motoneurons and in supporting cel ls, suggesting that altered expression of glutamate receptors underlie s the changed reflex responsivity. Copyright (C) 1996 IBRO. Published by Elsevier Science Ltd.