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Differences in inflammatory pain in nNOS-, iNOS- and eNOS-deficient mice.
Eur J Pain. 2007 Oct; 11(7):810-8.EJ

Abstract

To assess the relative importance of the isoforms of nitric oxide synthase (NOS) in inflammatory pain, we directly compared pain behaviour and paw thickness after intraplantar injection of complete Freund's adjuvant (CFA) in wild-type (WT) mice and in mice lacking either inducible (iNOS), endothelial (eNOS) or neuronal NOS (nNOS). In mice deficient for nNOS, thermal hyperalgesia was reduced by approximately 50% compared to wild type mice at 4 and 8h after CFA injection, and mechanical hypersensitivity was absent. The only change in pain behaviour in iNOS and eNOS deficient mice compared to WT mice was a more rapid recovery from thermal hyperalgesia. A compensatory up-regulation of nNOS in dorsal root ganglia (DRG) and spinal cords of iNOS and eNOS knockout mice was excluded using RT-PCR. However, an increase of iNOS gene expression was found in spinal cords of eNOS and nNOS deficient mice. To study the downstream effects of nNOS deficiency on DRG neurones, we assessed their immunoreactivity for calcitonin gene-related peptide (CGRP) and cytokines. We found a significant reduction in the CFA induced increase in CGRP immunoreactive neurones as well as in CGRP gene expression in nNOS deficient mice, whereas the percentage of cells immunopositive for tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) was unchanged. These results support the proposed role of nNOS in sensitization of DRG neurones, and might indicate that CGRP is involved in this process.

Authors+Show Affiliations

Department of Neurology, Julius-Maximilians-University, Josef-Schneider-Str 11, 97080, Würzburg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

17395508

Citation

Boettger, Michael Karl, et al. "Differences in Inflammatory Pain in nNOS-, iNOS- and eNOS-deficient Mice." European Journal of Pain (London, England), vol. 11, no. 7, 2007, pp. 810-8.
Boettger MK, Uceyler N, Zelenka M, et al. Differences in inflammatory pain in nNOS-, iNOS- and eNOS-deficient mice. Eur J Pain. 2007;11(7):810-8.
Boettger, M. K., Uceyler, N., Zelenka, M., Schmitt, A., Reif, A., Chen, Y., & Sommer, C. (2007). Differences in inflammatory pain in nNOS-, iNOS- and eNOS-deficient mice. European Journal of Pain (London, England), 11(7), 810-8.
Boettger MK, et al. Differences in Inflammatory Pain in nNOS-, iNOS- and eNOS-deficient Mice. Eur J Pain. 2007;11(7):810-8. PubMed PMID: 17395508.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differences in inflammatory pain in nNOS-, iNOS- and eNOS-deficient mice. AU - Boettger,Michael Karl, AU - Uceyler,Nurcan, AU - Zelenka,Marek, AU - Schmitt,Angelika, AU - Reif,Andreas, AU - Chen,Yong, AU - Sommer,Claudia, Y1 - 2007/03/28/ PY - 2006/07/12/received PY - 2006/11/28/revised PY - 2006/12/28/accepted PY - 2007/3/31/pubmed PY - 2007/12/6/medline PY - 2007/3/31/entrez SP - 810 EP - 8 JF - European journal of pain (London, England) JO - Eur J Pain VL - 11 IS - 7 N2 - To assess the relative importance of the isoforms of nitric oxide synthase (NOS) in inflammatory pain, we directly compared pain behaviour and paw thickness after intraplantar injection of complete Freund's adjuvant (CFA) in wild-type (WT) mice and in mice lacking either inducible (iNOS), endothelial (eNOS) or neuronal NOS (nNOS). In mice deficient for nNOS, thermal hyperalgesia was reduced by approximately 50% compared to wild type mice at 4 and 8h after CFA injection, and mechanical hypersensitivity was absent. The only change in pain behaviour in iNOS and eNOS deficient mice compared to WT mice was a more rapid recovery from thermal hyperalgesia. A compensatory up-regulation of nNOS in dorsal root ganglia (DRG) and spinal cords of iNOS and eNOS knockout mice was excluded using RT-PCR. However, an increase of iNOS gene expression was found in spinal cords of eNOS and nNOS deficient mice. To study the downstream effects of nNOS deficiency on DRG neurones, we assessed their immunoreactivity for calcitonin gene-related peptide (CGRP) and cytokines. We found a significant reduction in the CFA induced increase in CGRP immunoreactive neurones as well as in CGRP gene expression in nNOS deficient mice, whereas the percentage of cells immunopositive for tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) was unchanged. These results support the proposed role of nNOS in sensitization of DRG neurones, and might indicate that CGRP is involved in this process. SN - 1090-3801 UR - https://www.unboundmedicine.com/medline/citation/17395508/Differences_in_inflammatory_pain_in_nNOS__iNOS__and_eNOS_deficient_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1090-3801(07)00004-3 DB - PRIME DP - Unbound Medicine ER -