Differential contributions of NMDA and non-NMDA receptors to spinal Fos expression evoked by superficial tissue and muscle inflammation in the rat

The role of N-methyl-D-aspartate (NMDA) and non-NMDA receptors in the spina l cord in the transmission of nociceptive afferents from superficial tissue and muscle was studied by examining the effects of NMDA or non-NMDA recept or antagonists on Fos expression in the spinal dorsal hom. Muscle inflammat ion was induced by injection of turpentine oil into the gastrocnemius muscl e, whereas superficial tissue inflammation was induced by an intraplantar i njection of turpentine oil into the hindpaw. The NMDA receptor antagonist D L-2-amino-5-phosphonovaleric acid (AP-5), the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) or normal saline were intrathecally administered 15 min before an intramuscular or intraplantar injection of t urpentine oil. Muscle inflammation evoked expression of Fos-Eke immunoreact ive neurons staining in neurons that were predominantly distributed in the middle portions of laminae I-IIouter and the lateral portions of laminae V- VI of the ipsilateral dorsal horn at the spinal L-4-L-5. DNQX, but not AP-5 , significantly reduced the total number of Fos-Eke immunoreactive neurons evoked by muscle inflammation. In contrast, superficial tissue inflammation evoked expression of Fos-like immunoreactive neurons in the medial portion s of laminae and V-VI of the ipsilateral dorsal horn at the spinal L4-L5 th at was blocked by AP-5, but not by DNQX. Injection of normal saline did not influence the numbers of Fos-LI neurons. These results indicate that different glutamate receptors in the dorsal hor n of the spinal cord may mediate nociceptive input from superficial tissue (particularly skin) and muscle. DNQX receptors may mediate transmission of nociceptive information originating in muscle, while NMDA receptors may pre ferentially mediate transmission of nociceptive information originating in skin. (C) 2001 Published by Elsevier Science Ltd on behalf of IBRO.