N-methyl-D-aspartate R1 messenger RNA and [125I]MK-801 binding decrease in rat spinal cord after unilateral hind paw inflammation.

Abstract

Recent evidence suggests that N-methyl-D-aspartate receptors play an important role in the etiology and maintenance of chronic nociception. Previous studies have demonstrated that tissue injury or stimulation of nociceptive afferent projections results in the expansion of receptive fields, hyperalgesia and C-fiber-induced wind-up, events that can be inhibited by N-methyl-D-aspartate antagonists. This study examines the effect of unilateral hind paw inflammation on N-methyl-D-aspartate R1 messenger RNA and [125I]dizocilpine maleate binding in the L4-L5 segments of the lumbar spinal cord of rats. Spinal cords were examined at 7.5 h, three, seven and 20 days after injection of the left hind paw with 120 microliters of complete Freund's adjuvant. N-methyl-D-aspartate R1 messenger RNA, as measured with in situ hybridization, was observed to decrease bilaterally in laminae I, II and X of the lumbar spinal cord. This decrease was evident in laminae I and II at 7.5 h and three days after hind paw injection. In lamina X, a postinjection decrease in hybridization signal was observed at 7.5 h and seven days. A bilateral decrease in [125I]dizocilpine maleate binding was observed in laminae I and II at three, seven and 20 days after paw injection. This observed decrease in binding at the N-methyl-D-aspartate receptor suggests a compensatory mechanism by which N-methyl-D-aspartate-mediated nociceptive events may be modulated.