Induction of spinal long-term synaptic potentiation is sensitive to inhibition of neuronal NOS in L5 spinal nerve-transected rats.

Abstract

The role of neuronal nitric oxide synthase (nNOS) in the central mechanism of neuropathic pain and long-term potentiation (LTP) of peripheral afferents remains obscure. The current study investigated the effect of intrathecal application of 7-nitroindazole (7-NI), a selective nNOS inhibitor (8.15 µg/5µl), on mechanical allodynia on day 14 after L5 spinal nerve transection. Furthermore, using in vivo single unit extracellular recording, we examined the effect of 7-NI on the induction of LTP of Aδ- and C-fiber-evoked responses. We have demonstrated that 7-NI attenuates nerve-injury-evoked mechanical allodynia. Additionally, our electrophysiological study has shown that the spinal administration of 7-NI significantly inhibits the induction of the LTP of Aδ- and C-fiber-evoked responses on day 14 after neuropathy. These data suggest that activation of nNOS may be crucial for the induction of the spinal LTP of Aδ- and C-fiber-evoked responses following peripheral nerve damage.