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Intrathecal interleukin-1beta administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord.
Brain Res. 2004 Jul 23; 1015(1-2):145-53.BR

Abstract

The effect of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) on the inducible nitric oxide synthase-nitric oxide (iNOS-NO) cascade in nociceptive signal transduction was examined in the intact rat spinal cord. All rats were implanted with an intrathecal (i.t.) catheter; some were also implanted with an i.t. microdialysis probe. The paw withdrawal latency to radiant heat was used to assess thermal hyperalgesia. The iNOS protein expression in the spinal cord dorsal horn was examined by western blot analysis and NOS activity assay. NO production in the CSF dialysate was also measured. IL-1beta i.t. (100 ng) produced thermal hyperalgesia from 4 to 24 h after i.t. injection. The iNOS protein expression was induced at 4 h after i.t. IL-1beta injection, peaked at the 6th hour, and disappeared at 24 h. The iNOS activity showed a similar time-dependent change as the iNOS protein expression. NO release increased by 1.1- to 1.9-fold between 4 and 12 h, also with a peak at the 6th hour, after i.t. IL-1beta administration. Pretreatment with the iNOS inhibitor 1400W (10 microg, i.t.) 1 h before i.t. IL-1beta injection prevented all the responses of IL-1beta. Neither 1400W nor artificial CSF (aCSF) affected the thermal nociceptive threshold and NO production. These results demonstrate that i.t. administration of IL-1beta induced thermal hyperalgesia by activating the iNOS-NO cascade in the rat spinal cord. On the basis of the present findings, we suggest that i.t. administration of iNOS inhibitors may have potential in the treatment of inflammatory and neuropathic pain syndromes.

Authors+Show Affiliations

Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.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
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15223378

Citation

Sung, Chun-Sung, et al. "Intrathecal Interleukin-1beta Administration Induces Thermal Hyperalgesia By Activating Inducible Nitric Oxide Synthase Expression in the Rat Spinal Cord." Brain Research, vol. 1015, no. 1-2, 2004, pp. 145-53.
Sung CS, Wen ZH, Chang WK, et al. Intrathecal interleukin-1beta administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord. Brain Res. 2004;1015(1-2):145-53.
Sung, C. S., Wen, Z. H., Chang, W. K., Ho, S. T., Tsai, S. K., Chang, Y. C., & Wong, C. S. (2004). Intrathecal interleukin-1beta administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord. Brain Research, 1015(1-2), 145-53.
Sung CS, et al. Intrathecal Interleukin-1beta Administration Induces Thermal Hyperalgesia By Activating Inducible Nitric Oxide Synthase Expression in the Rat Spinal Cord. Brain Res. 2004 Jul 23;1015(1-2):145-53. PubMed PMID: 15223378.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intrathecal interleukin-1beta administration induces thermal hyperalgesia by activating inducible nitric oxide synthase expression in the rat spinal cord. AU - Sung,Chun-Sung, AU - Wen,Zhi-Hong, AU - Chang,Wen-Kuei, AU - Ho,Shung-Tai, AU - Tsai,Shen-Kou, AU - Chang,Yi-Chen, AU - Wong,Chih-Shung, PY - 2004/04/20/accepted PY - 2004/6/30/pubmed PY - 2004/10/16/medline PY - 2004/6/30/entrez SP - 145 EP - 53 JF - Brain research JO - Brain Res VL - 1015 IS - 1-2 N2 - The effect of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) on the inducible nitric oxide synthase-nitric oxide (iNOS-NO) cascade in nociceptive signal transduction was examined in the intact rat spinal cord. All rats were implanted with an intrathecal (i.t.) catheter; some were also implanted with an i.t. microdialysis probe. The paw withdrawal latency to radiant heat was used to assess thermal hyperalgesia. The iNOS protein expression in the spinal cord dorsal horn was examined by western blot analysis and NOS activity assay. NO production in the CSF dialysate was also measured. IL-1beta i.t. (100 ng) produced thermal hyperalgesia from 4 to 24 h after i.t. injection. The iNOS protein expression was induced at 4 h after i.t. IL-1beta injection, peaked at the 6th hour, and disappeared at 24 h. The iNOS activity showed a similar time-dependent change as the iNOS protein expression. NO release increased by 1.1- to 1.9-fold between 4 and 12 h, also with a peak at the 6th hour, after i.t. IL-1beta administration. Pretreatment with the iNOS inhibitor 1400W (10 microg, i.t.) 1 h before i.t. IL-1beta injection prevented all the responses of IL-1beta. Neither 1400W nor artificial CSF (aCSF) affected the thermal nociceptive threshold and NO production. These results demonstrate that i.t. administration of IL-1beta induced thermal hyperalgesia by activating the iNOS-NO cascade in the rat spinal cord. On the basis of the present findings, we suggest that i.t. administration of iNOS inhibitors may have potential in the treatment of inflammatory and neuropathic pain syndromes. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/15223378/Intrathecal_interleukin_1beta_administration_induces_thermal_hyperalgesia_by_activating_inducible_nitric_oxide_synthase_expression_in_the_rat_spinal_cord_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006899304007115 DB - PRIME DP - Unbound Medicine ER -