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Regulation of spinal neuroimmune responses by prolonged morphine treatment in a rat model of cancer induced bone pain.
Brain Res. 2010 Apr 22; 1326:162-73.BR

Abstract

Cancer induced bone pain (CIBP) is a major clinical problem. Although opioids remain the principal axis in drug therapies for CIBP, their sustained application is known to induce cellular and molecular adaptations including enhanced neuroimmune reactivity. This is generally characterized by glial activation and proinflammatory cytokine production which frequently results in pharmacological tolerance. This research was performed to investigate spinal neuroimmune responses after prolonged systemic morphine treatment in a rat model of CIBP. The model was established using a unilateral intra-tibia injection of Walker 256 mammary gland carcinoma cells. Subcutaneous morphine was repeatedly administered from postoperative days 14 to 19. Mechanical allodynia to von Frey filaments and ambulatory pain scores were recorded to investigate changes of nociceptive behaviors. Spinal glial activation was detected by immunohistochemistry and real-time PCR; the production of proinflammatory cytokines (IL-1beta and TNF-alpha) was examined through real-time PCR and ELISA. Results showed that chronic morphine use failed to elicit analgesic tolerance in the rat CIBP model. Moreover, the treatment had no significant influence on the activated spinal glia morphology, cell density and expression of special cytomembrane markers, whereas it significantly down-regulated the local proinflammatory cytokine production at the mRNA and protein level. Collectively, these data suggest that chronic morphine treatment in CIBP is not concomitant with pharmacological tolerance, at least partially because the treatment fails to amplify spinal neuroimmune responses.

Authors+Show Affiliations

Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

20176002

Citation

Cao, Fei, et al. "Regulation of Spinal Neuroimmune Responses By Prolonged Morphine Treatment in a Rat Model of Cancer Induced Bone Pain." Brain Research, vol. 1326, 2010, pp. 162-73.
Cao F, Gao F, Xu AJ, et al. Regulation of spinal neuroimmune responses by prolonged morphine treatment in a rat model of cancer induced bone pain. Brain Res. 2010;1326:162-73.
Cao, F., Gao, F., Xu, A. J., Chen, Z. J., Chen, S. S., Yang, H., Yu, H. H., Mei, W., Liu, X. J., Xiao, X. P., Yang, S. B., Tian, X. B., Wang, X. R., & Tian, Y. K. (2010). Regulation of spinal neuroimmune responses by prolonged morphine treatment in a rat model of cancer induced bone pain. Brain Research, 1326, 162-73. https://doi.org/10.1016/j.brainres.2010.02.039
Cao F, et al. Regulation of Spinal Neuroimmune Responses By Prolonged Morphine Treatment in a Rat Model of Cancer Induced Bone Pain. Brain Res. 2010 Apr 22;1326:162-73. PubMed PMID: 20176002.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of spinal neuroimmune responses by prolonged morphine treatment in a rat model of cancer induced bone pain. AU - Cao,Fei, AU - Gao,Feng, AU - Xu,Ai-Jun, AU - Chen,Zhi-Jun, AU - Chen,Sha-Sha, AU - Yang,Hui, AU - Yu,Hong-Hui, AU - Mei,Wei, AU - Liu,Xi-Jiang, AU - Xiao,Xing-Peng, AU - Yang,Shao-Bing, AU - Tian,Xue-Bi, AU - Wang,Xue-Ren, AU - Tian,Yu-Ke, Y1 - 2010/02/20/ PY - 2009/11/05/received PY - 2010/02/08/revised PY - 2010/02/08/accepted PY - 2010/2/24/entrez PY - 2010/2/24/pubmed PY - 2010/6/26/medline SP - 162 EP - 73 JF - Brain research JO - Brain Res VL - 1326 N2 - Cancer induced bone pain (CIBP) is a major clinical problem. Although opioids remain the principal axis in drug therapies for CIBP, their sustained application is known to induce cellular and molecular adaptations including enhanced neuroimmune reactivity. This is generally characterized by glial activation and proinflammatory cytokine production which frequently results in pharmacological tolerance. This research was performed to investigate spinal neuroimmune responses after prolonged systemic morphine treatment in a rat model of CIBP. The model was established using a unilateral intra-tibia injection of Walker 256 mammary gland carcinoma cells. Subcutaneous morphine was repeatedly administered from postoperative days 14 to 19. Mechanical allodynia to von Frey filaments and ambulatory pain scores were recorded to investigate changes of nociceptive behaviors. Spinal glial activation was detected by immunohistochemistry and real-time PCR; the production of proinflammatory cytokines (IL-1beta and TNF-alpha) was examined through real-time PCR and ELISA. Results showed that chronic morphine use failed to elicit analgesic tolerance in the rat CIBP model. Moreover, the treatment had no significant influence on the activated spinal glia morphology, cell density and expression of special cytomembrane markers, whereas it significantly down-regulated the local proinflammatory cytokine production at the mRNA and protein level. Collectively, these data suggest that chronic morphine treatment in CIBP is not concomitant with pharmacological tolerance, at least partially because the treatment fails to amplify spinal neuroimmune responses. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/20176002/Regulation_of_spinal_neuroimmune_responses_by_prolonged_morphine_treatment_in_a_rat_model_of_cancer_induced_bone_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(10)00386-0 DB - PRIME DP - Unbound Medicine ER -