In the present study, we investigated the role of spinal
nitric oxide (NO) in rat
pain-related behaviors induced by the
venom of scorpion Buthus martensi Karsch (BmK). The results showed that the number of neuronal
NO synthase (nNOS) positive neurons significantly increased in superficial (I-II), deep (V-VI) dorsal horn laminae and the ventral gray laminae (VII-X), but not in the nucleus proprius (III and IV) of bilateral L4-L5 lumbar spinal cord after unilateral intraplantar injection of BmK
venom from 2h to 7d. This increase on the ipsilateral side to BmK
venom injection was always greater than that on the contralateral side. Western blotting analysis confirmed that spinal nNOS expression was significantly up-regulated following BmK
venom administration. In addition, intrathecal delivery of
N(omega)-nitro-l-arginine methyl ester hydrochloride (
l-NAME; a NOS inhibitor) before intraplantar injection of BmK
venom by 10 min significantly attenuated spontaneous nociceptive responses and prevented the development of primary
thermal hyperalgesia as well as bilateral
mechanical hyperalgesia.
Intrathecal injection of
l-NAME could also partially inhibit BmK
venom-induced c-Fos expression in lumbar spinal cord at 2 h. Thus, the results suggest that spinal NO as a critical mediator is involved in various
pain-related behaviors and c-Fos expression induced by BmK
venom in rats.