Bahari, ZahraManaheji, HomaHosseinmardi, NargesMeftahi, Gholam HosseinSadeghi, MehdiDanialy, SamiraNoorbakhsh, Seyed Mohammad2014-11-252014-11-252014-07-141611-2156http://hdl.handle.net/2003/3370810.17877/DE290R-6845The 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.enEXCLI Journal ; Vol. 13, 2014neuropathic painnNOSLTPdorsal horn610article (journal)