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Peri-sciatic administration of recombinant rat TNF-alpha induces mechanical allodynia via upregulation of TNF-alpha in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway.
Exp Neurol. 2007 Jun; 205(2):471-84.EN

Abstract

Previous studies have shown that tumor necrosis factor-alpha (TNF-alpha) and TNF receptor 1 (TNFR1) in dorsal root ganglia (DRG) and in spinal dorsal horn are upregulated after nerve injury and that many TNF-alpha-containing neurons overexpress TNFR1. In the present study, we found that peri-sciatic administration of rat recombinant TNF-alpha (rrTNF) at the concentrations of 10, 100 and 1000 pg/ml (daily for 2 days) induced mechanical allodynia in bilateral hindpaws, lasting for about 20 days. The immunoreactivity (IR) of TNF-alpha and TNFR1 in the ipsilateral (but not in the contralateral) L4 and L5 DRGs increased significantly on day 1 and day 3 after administration of rrTNF, respectively. Double immunofluorescence staining revealed that in DRGs the increased TNF-alpha-IR was mainly in neuronal cells and with a lesser extent in satellite glial cells, while the upregulation of TNFR1-IR was almost restricted at neuronal cells. TNF-alpha-IR but not TNFR1-IR also increased in bilateral lumbar spinal dorsal horn from day 3 to day 14, which was observed in astrocytes, microglias and neurons. In addition, a progressive infiltration of monocyte/macrophages and T lymphocytes in the ipsilateral L5 DRG and sciatic nerve was observed, starting on day 2 following administration of rrTNF. Intrathecal delivery of PDTC (8.2 ng in 10 microl volume), a nuclear factor-kappa B (NF-kappaB) inhibitor, 30 min before each rrTNF administration blocked mechanical allodynia completely and inhibited the upregulation of TNF-alpha-IR and TNFR1-IR substantially. The results suggest that peri-sciatic administration of rrTNF may induce mechanical allodynia by an autocrine mechanism via activation of the NF-kappaB pathway.

Authors+Show Affiliations

Pain Research Center, Department of Physiology, Zhongshan Medical School of Sun Yat-Sen University, 74 Zhongshan Rd. 2, Guangzhou, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17459378

Citation

Wei, Xu-Hong, et al. "Peri-sciatic Administration of Recombinant Rat TNF-alpha Induces Mechanical Allodynia Via Upregulation of TNF-alpha in Dorsal Root Ganglia and in Spinal Dorsal Horn: the Role of NF-kappa B Pathway." Experimental Neurology, vol. 205, no. 2, 2007, pp. 471-84.
Wei XH, Zang Y, Wu CY, et al. Peri-sciatic administration of recombinant rat TNF-alpha induces mechanical allodynia via upregulation of TNF-alpha in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway. Exp Neurol. 2007;205(2):471-84.
Wei, X. H., Zang, Y., Wu, C. Y., Xu, J. T., Xin, W. J., & Liu, X. G. (2007). Peri-sciatic administration of recombinant rat TNF-alpha induces mechanical allodynia via upregulation of TNF-alpha in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway. Experimental Neurology, 205(2), 471-84.
Wei XH, et al. Peri-sciatic Administration of Recombinant Rat TNF-alpha Induces Mechanical Allodynia Via Upregulation of TNF-alpha in Dorsal Root Ganglia and in Spinal Dorsal Horn: the Role of NF-kappa B Pathway. Exp Neurol. 2007;205(2):471-84. PubMed PMID: 17459378.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peri-sciatic administration of recombinant rat TNF-alpha induces mechanical allodynia via upregulation of TNF-alpha in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway. AU - Wei,Xu-Hong, AU - Zang,Ying, AU - Wu,Chang-You, AU - Xu,Ji-Tian, AU - Xin,Wen-Jun, AU - Liu,Xian-Guo, Y1 - 2007/03/23/ PY - 2006/10/11/received PY - 2007/02/22/revised PY - 2007/03/06/accepted PY - 2007/4/27/pubmed PY - 2007/7/11/medline PY - 2007/4/27/entrez SP - 471 EP - 84 JF - Experimental neurology JO - Exp Neurol VL - 205 IS - 2 N2 - Previous studies have shown that tumor necrosis factor-alpha (TNF-alpha) and TNF receptor 1 (TNFR1) in dorsal root ganglia (DRG) and in spinal dorsal horn are upregulated after nerve injury and that many TNF-alpha-containing neurons overexpress TNFR1. In the present study, we found that peri-sciatic administration of rat recombinant TNF-alpha (rrTNF) at the concentrations of 10, 100 and 1000 pg/ml (daily for 2 days) induced mechanical allodynia in bilateral hindpaws, lasting for about 20 days. The immunoreactivity (IR) of TNF-alpha and TNFR1 in the ipsilateral (but not in the contralateral) L4 and L5 DRGs increased significantly on day 1 and day 3 after administration of rrTNF, respectively. Double immunofluorescence staining revealed that in DRGs the increased TNF-alpha-IR was mainly in neuronal cells and with a lesser extent in satellite glial cells, while the upregulation of TNFR1-IR was almost restricted at neuronal cells. TNF-alpha-IR but not TNFR1-IR also increased in bilateral lumbar spinal dorsal horn from day 3 to day 14, which was observed in astrocytes, microglias and neurons. In addition, a progressive infiltration of monocyte/macrophages and T lymphocytes in the ipsilateral L5 DRG and sciatic nerve was observed, starting on day 2 following administration of rrTNF. Intrathecal delivery of PDTC (8.2 ng in 10 microl volume), a nuclear factor-kappa B (NF-kappaB) inhibitor, 30 min before each rrTNF administration blocked mechanical allodynia completely and inhibited the upregulation of TNF-alpha-IR and TNFR1-IR substantially. The results suggest that peri-sciatic administration of rrTNF may induce mechanical allodynia by an autocrine mechanism via activation of the NF-kappaB pathway. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/17459378/Peri_sciatic_administration_of_recombinant_rat_TNF_alpha_induces_mechanical_allodynia_via_upregulation_of_TNF_alpha_in_dorsal_root_ganglia_and_in_spinal_dorsal_horn:_the_role_of_NF_kappa_B_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(07)00101-X DB - PRIME DP - Unbound Medicine ER -