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Role of astrocytic S100beta in behavioral hypersensitivity in rodent models of neuropathic pain.
Neuroscience. 2006 Jul 07; 140(3):1003-10.N

Abstract

S100beta is a calcium-binding peptide produced mainly by astrocytes that exerts paracrine and autocrine effects on neurons and glia. We have previously shown that S100beta is markedly elevated at the mRNA level in the spinal cord following peripheral inflammation, intraplantar administration of complete Freund's adjuvant in the rat. The purpose of the present study was to further investigate the role of astrocytic S100beta in mediating behavioral hypersensitivity in rodent models of persistent pain. First, we assessed the lumbar spinal cord expression of S100beta at the mRNA and protein level using real-time RT-PCR, Western blot and immunohistochemistry analysis following L5 spinal nerve transection in rats, a rodent model of neuropathic pain. Second, we assessed behavioral hypersensitivity (mechanical allodynia) in wild type and genetically modified mice lacking or overexpressing S100beta following L5 spinal nerve transection. Third, we assessed the expression level of S100beta protein in the CD1 wild type mice after nerve injury. We report that lumbar spinal S100beta mRNA steadily increased from days 4-28 after nerve injury. S100beta protein in the lumbar spinal cord was significantly increased in both rats and mice at day 14 following nerve injury as compared with sham control groups. S100beta genetically deficient mice displayed significantly increased tactile thresholds (reduced response to non-noxious stimuli) after nerve injury as compared with the wild type group. S100beta overexpressing mice displayed significantly decreased tactile threshold responses (enhanced response to non-noxious stimuli). Together, these results from both series of experiments using a peripheral nerve injury model in two different species implicate the involvement of glial-derived S100beta in the pathophysiology of neuropathic pain.

Authors+Show Affiliations

Department of Anesthesiology, Dartmouth Medical School, Lebanon, NH 03756, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16600520

Citation

Tanga, F Y., et al. "Role of Astrocytic S100beta in Behavioral Hypersensitivity in Rodent Models of Neuropathic Pain." Neuroscience, vol. 140, no. 3, 2006, pp. 1003-10.
Tanga FY, Raghavendra V, Nutile-McMenemy N, et al. Role of astrocytic S100beta in behavioral hypersensitivity in rodent models of neuropathic pain. Neuroscience. 2006;140(3):1003-10.
Tanga, F. Y., Raghavendra, V., Nutile-McMenemy, N., Marks, A., & Deleo, J. A. (2006). Role of astrocytic S100beta in behavioral hypersensitivity in rodent models of neuropathic pain. Neuroscience, 140(3), 1003-10.
Tanga FY, et al. Role of Astrocytic S100beta in Behavioral Hypersensitivity in Rodent Models of Neuropathic Pain. Neuroscience. 2006 Jul 7;140(3):1003-10. PubMed PMID: 16600520.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of astrocytic S100beta in behavioral hypersensitivity in rodent models of neuropathic pain. AU - Tanga,F Y, AU - Raghavendra,V, AU - Nutile-McMenemy,N, AU - Marks,A, AU - Deleo,J A, PY - 2005/12/20/received PY - 2006/02/07/revised PY - 2006/02/23/accepted PY - 2006/4/8/pubmed PY - 2006/9/9/medline PY - 2006/4/8/entrez SP - 1003 EP - 10 JF - Neuroscience JO - Neuroscience VL - 140 IS - 3 N2 - S100beta is a calcium-binding peptide produced mainly by astrocytes that exerts paracrine and autocrine effects on neurons and glia. We have previously shown that S100beta is markedly elevated at the mRNA level in the spinal cord following peripheral inflammation, intraplantar administration of complete Freund's adjuvant in the rat. The purpose of the present study was to further investigate the role of astrocytic S100beta in mediating behavioral hypersensitivity in rodent models of persistent pain. First, we assessed the lumbar spinal cord expression of S100beta at the mRNA and protein level using real-time RT-PCR, Western blot and immunohistochemistry analysis following L5 spinal nerve transection in rats, a rodent model of neuropathic pain. Second, we assessed behavioral hypersensitivity (mechanical allodynia) in wild type and genetically modified mice lacking or overexpressing S100beta following L5 spinal nerve transection. Third, we assessed the expression level of S100beta protein in the CD1 wild type mice after nerve injury. We report that lumbar spinal S100beta mRNA steadily increased from days 4-28 after nerve injury. S100beta protein in the lumbar spinal cord was significantly increased in both rats and mice at day 14 following nerve injury as compared with sham control groups. S100beta genetically deficient mice displayed significantly increased tactile thresholds (reduced response to non-noxious stimuli) after nerve injury as compared with the wild type group. S100beta overexpressing mice displayed significantly decreased tactile threshold responses (enhanced response to non-noxious stimuli). Together, these results from both series of experiments using a peripheral nerve injury model in two different species implicate the involvement of glial-derived S100beta in the pathophysiology of neuropathic pain. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/16600520/Role_of_astrocytic_S100beta_in_behavioral_hypersensitivity_in_rodent_models_of_neuropathic_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(06)00304-6 DB - PRIME DP - Unbound Medicine ER -