Effect of spinal cord transection on N-methyl-D-aspartate receptors in thecord

Spinal cord injury can lead to an exaggeration of transmission through spin al pathways, resulting in muscle spasticity, chronic pain, and abnormal con trol of blood pressure and bladder function. These conditions are mediated, in part, by N-methyl-D-aspartate (NMDA) receptors on spinal neurons, but t he effects of cord injury on the expression or function of these receptors is unknown, Therefore, antibodies to the NMDA-R1 receptor subunit and bindi ng of [H-3]MK-801 were used to assess NMDA receptors in the spinal cord, Re ceptor density in rats with intact spinal cords was compared to that in rat s 1 and 2 weeks after spinal cord transection (SCT) at the mid-thoracic lev el, At 1 and 2 weeks after SCT, [H-3]MK-801 binding was reduced in most lam inae in cord segments caudal to the injury, whereas no decrease in amount o f R1 subunit immunoreactivity was observed, No significant changes in [H-3] MK-801 binding and NMDA-R1 immunoreactivity could be seen rostral to the tr ansection, Since [H-3]MK-801 binding requires an open ion channel, the disc repancy between [H-3]MK-801 binding and immunocytochemistry may indicate a loss of functional receptors without a consistent change in their total num ber, Therefore, the exaggerated reflexes that are well established in rats 2 weeks after cord injury must be mediated by a mechanism that withstands a ttenuation of NMDA receptor function.