Interleukin-1β Induces Long-Term Potentiation of C-Fiber Evoked Field Potentials in Spinal dorsal Horn in Rats with Neuropathic Pain

Yi Zhong, Li-Jun Zhou, Wen-Jie Ren, Wen-jun Xin, Yong-Yong Li, Tong Zhang, Xian-Guo Liu*
Pain Research Center and Department of Physiology, Zhongshan Medical School of Sun Yat-sen University, 510080 Guangzhou, China.

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© 2009 Zhong et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Pain Research Center and Department of Physiology, Zhongshan Medical School of Sun Yat-senv University, 510080 Guangzhou, China; Tel: 0086-20-87331956; E-mail:


Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β), impairs long-term potentiation (LTP) in hippocampus, a synaptic model of memory, while in spinal dorsal horn TNF-α is found to induce LTP of C-fiber evoked field potentials in rats with nerve injury. In the present work the role of IL-1β in the spinal LTP of C-fiber evoked field potentials, which is important for pathological pain, was investigated in both physiological and pathological conditions. We found that spinal application of IL-1β at the concentrations up to 500 ng/ml affected neither basal synaptic transmission mediated by C-fiber nor spinal LTP induced by tetanic stimulation in intact rats. In rats with neuropathic pain produced by spared nerve injury (SNI) or lumbar 5 ventral root transection (L5 VRT), however, IL- 1β at a low concentration (5 ng/ml) induced LTP of C-fiber evoked field potentials. Pretreatment with either p38 MAPK inhibitor (SB203580) or NF-κB inhibitor (PDTC) but not with JNK inhibitor (SP600125) completely blocked LTP induced by IL-1β in SNI rats. Taken together, the results indicated that exogenous IL-1β might induce spinal LTP only in rats with nerve injury but not in intact rats. The differential effects of proinflammatory cytokines on synaptic plasticity in spinal dorsal horn and in hippocampus may be clinically significant.

Keywords: Interleukine-1, long-Term Potentiation, Spinal Dorsal Horn.