| Intrathecal interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibits an anti-allodynic action in a rat model of neuropathic pain. | |
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MedLine Citation:
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PMID: 11246166 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The expression of interleukin-1beta and tumor necrosis factor has previously been shown to be up-regulated in the spinal cord of several rat mononeuropathy models. This present study was undertaken to determine whether blocking the action of central interleukin-1beta and tumor necrosis factor attenuates mechanical allodynia in a gender-specific manner in a rodent L5 spinal nerve transection model of neuropathic pain, and whether this inhibition occurs via down-regulation of the central cytokine cascade or blockade of glial activation. Interleukin-1 receptor antagonist or soluble tumor necrosis factor receptor was administered intrathecally via lumbar puncture to male Holtzman rats in a preventative pain strategy, in which therapy was initiated 1h prior to surgery. Administration of soluble tumor necrosis factor receptor attenuated mechanical allodynia, while interleukin-1 receptor antagonist alone was unable to decrease allodynia. Interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor, administered to both male and female rats in a preventative pain strategy, significantly reduced mechanical allodynia in a dose-dependent manner (P<0.01). The magnitude of attenuation in allodynia was similar in both males and females. Immunohistochemistry on L5 spinal cord revealed similar astrocytic and microglial activation regardless of treatment. At days 3 and 7 post-transection, animals receiving daily interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibited significantly less interleukin-6, but not interleukin-1beta, in the L5 spinal cord compared to vehicle-treated animals. In an existing pain paradigm, in which treatment was initiated on day 7 post-transection, interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor attenuated mechanical allodynia (P<0.05) in male rats. These findings further support a role for central interleukin-1beta and tumor necrosis factor in the development and maintenance of neuropathic pain through induction of a proinflammatory cytokine cascade. |
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Authors:
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S Sweitzer; D Martin; J A DeLeo |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Neuroscience Volume: 103 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 2001 |
Date Detail:
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Created Date: 2001-03-14 Completed Date: 2001-06-14 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: United States |
Other Details:
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Languages: eng Pagination: 529-39 Citation Subset: IM |
Affiliation:
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Department of Pharmacology and Toxicology, Hinman Box 7650, Dartmouth College, Hanover, NH 03755, USA. sarah.sweitzer@dartmouth.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Disease Models, Animal Drug Therapy, Combination Female Immunoglobulin G / pharmacology* Injections, Spinal Interleukin 1 Receptor Antagonist Protein Interleukin-1 / metabolism Interleukin-6 / metabolism Male Neuralgia / drug therapy*, immunology, metabolism* Neuroglia / immunology, metabolism Neurons / immunology, metabolism Rats Rats, Sprague-Dawley Receptors, Tumor Necrosis Factor Sex Factors Sialoglycoproteins / pharmacology* Spinal Cord / cytology, metabolism, physiology Spinal Nerves / physiopathology, surgery Tumor Necrosis Factor-alpha / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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DA11276/DA/NIDA NIH HHS; F31 DA05969/DA/NIDA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Immunoglobulin G; 0/Interleukin 1 Receptor Antagonist Protein; 0/Interleukin-1; 0/Interleukin-6; 0/Receptors, Tumor Necrosis Factor; 0/Sialoglycoproteins; 0/Tumor Necrosis Factor-alpha; 185243-69-0/TNFR-Fc fusion protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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