Tumor necrosis factor-α induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn in rats with nerve injury: The role of NF-kappa B, JNK and p38 MAPK Export

@article{citeulike:4744379, abstract = {Compelling evidence has shown that in hippocampus tumor necrosis factor α (TNF-α) at pathological concentration inhibits long-term potentiation (LTP), a synaptic model of learning and memory. In the present work we investigated the role of TNF-α in LTP of C-fiber evoked field potentials in spinal dorsal horn, which is relevant to pathological pain. We showed that spinal application of TNF-α affected neither basal synaptic transmission mediated by C-fibers nor spinal LTP of C-fiber evoked field potentials induced by tetanic stimulation in intact rats. However, in rats with neuropathic pain, produced by either lumbar 5 ventral root transection (L5 VRT) or spared nerve injury (SNI), spinal application of TNF-α induced LTP of C-fiber evoked field potentials. Spinal application of JNK inhibitor (SP600125) or p38 MAPK inhibitor (SB203580) did not affect the spinal LTP induced by tetanic stimulation in intact rats, but completely blocked LTP induced by TNF-α in L5 VRT rats. NF-kappa B (NF-κB) inhibitor (PDTC) also blocked LTP induced by TNF-α. These results suggest that TNF-α and its downstream molecules may have no acute effect on spinal synaptic transmission in intact animals and induce LTP in rats with neuropathic pain produced by nerve injury.}, author = {Liu, Yan-Ling and Zhou, Li-Jun and Hu, Neng-Wei and Xu, Ji-Tian and Wu, Chang-You and Zhang, Tong and Li, Yong-Yong and Liu, Xian-Guo}, citeulike-article-id = {4744379}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.neuropharm.2006.09.011}, citeulike-linkout-1 = {http://linkinghub.elsevier.com/retrieve/pii/S0028390806003339}, doi = {10.1016/j.neuropharm.2006.09.011}, issn = {00283908}, journal = {Neuropharmacology}, keywords = {c-fibers, tnf-a}, month = {March}, number = {3}, pages = {708--715}, posted-at = {2009-06-04 13:29:59}, priority = {3}, title = {Tumor necrosis factor-α induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn in rats with nerve injury: The role of NF-kappa B, JNK and p38 MAPK}, url = {http://dx.doi.org/10.1016/j.neuropharm.2006.09.011}, volume = {52}, year = {2007} }

TY - JOUR ID - citeulike:4744379 L3 - citeulike-article-id:4744379 N2 - Compelling evidence has shown that in hippocampus tumor necrosis factor α (TNF-α) at pathological concentration inhibits long-term potentiation (LTP), a synaptic model of learning and memory. In the present work we investigated the role of TNF-α in LTP of C-fiber evoked field potentials in spinal dorsal horn, which is relevant to pathological pain. We showed that spinal application of TNF-α affected neither basal synaptic transmission mediated by C-fibers nor spinal LTP of C-fiber evoked field potentials induced by tetanic stimulation in intact rats. However, in rats with neuropathic pain, produced by either lumbar 5 ventral root transection (L5 VRT) or spared nerve injury (SNI), spinal application of TNF-α induced LTP of C-fiber evoked field potentials. Spinal application of JNK inhibitor (SP600125) or p38 MAPK inhibitor (SB203580) did not affect the spinal LTP induced by tetanic stimulation in intact rats, but completely blocked LTP induced by TNF-α in L5 VRT rats. NF-kappa B (NF-κB) inhibitor (PDTC) also blocked LTP induced by TNF-α. These results suggest that TNF-α and its downstream molecules may have no acute effect on spinal synaptic transmission in intact animals and induce LTP in rats with neuropathic pain produced by nerve injury. IS - 3 JF - Neuropharmacology SN - 00283908 EP - 715 TI - Tumor necrosis factor-α induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn in rats with nerve injury: The role of NF-kappa B, JNK and p38 MAPK VL - 52 SP - 708 KW - c-fibers KW - tnf-a AU - Liu, Yan-Ling AU - Zhou, Li-Jun AU - Hu, Neng-Wei AU - Xu, Ji-Tian AU - Wu, Chang-You AU - Zhang, Tong AU - Li, Yong-Yong AU - Liu, Xian-Guo PY - 2007/03// UR - http://dx.doi.org/10.1016/j.neuropharm.2006.09.011 ER -