Abstract
Spinal cord injury (SCI) impairs descending glutamatergic neurotransmission reaching ventral motor neurons (VMN). Previously we reported up-regulation of NMDA receptor subunits NR1 and NR2A mRNAs in VMN caudal to the lesion site 24 h after SCI. The absence of effect rostral to the injury site suggested that injury-induced loss of descending activity might be involved. To test this hypothesis, we blocked axonal conduction by focal injection of tetrodotoxin into the spinal cord. We found increased NR1 and NR2A mRNAs in VMN similar in extent to that seen after SCI. Thus, the increase in NMDA subunit mRNAs may be ‘inactivity dependent’ and associated with reorganization of the spinal cord in response to loss of descending innervation.
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