Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain

Andreas Hald; Ming Ding; Kristoffer Lihme Egerod; Rikke Rie Hansen; Dorthe Konradsen; Stine G. Jørgensen; Baris Atalay; Arafat Nasser; Ole Jannik Bjerrum; Anne-Marie Heegaard

doi:10.1016/j.pbb.2008.04.021

Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain

Andreas Hald, Ming Ding, Kristoffer Lihme Egerod, Rikke Rie Hansen, Dorthe Konradsen, Stine G. Jørgensen, Baris Atalay, Arafat Nasser, Ole Jannik Bjerrum, Anne-Marie Heegaard

25 Citations (Scopus)

Abstract

Pain due to bone malignancies is one of the most difficult types of cancer pain to fully control and may further decrease the patients' quality of life. Animal models of chronic pain conditions resulting from peripheral inflammatory reactions or nerve injuries are responsive to treatment with cannabinoid agonists. However, the use of cannabinoid agonists in humans may be hampered by CNS related side effects and development of tolerance. In the present study, we investigated the effect of repeated low dose administration of the synthetic cannabinoid agonist WIN 55,212-2 on bone cancer pain and neuropathic pain in mice. In addition, we investigated the development of CNS related side effects and tolerance. We found that 0.5 mg/kg/day for 18 days reduced pain related behavior and expression of spinal glial fibrillary acidic protein in the bone cancer pain model but not in the neuropathic pain model. Furthermore, this treatment strategy was not found to induce measurable CNS related side effects or tolerance. Cancer cell viability assays and bone volume fraction assessed by micro computed tomography (microCT) demonstrated that these effects were not due to changes in cancer progression. The difference in WIN 55,212-2 efficacy between the bone cancer and neuropathic pain models may reflect the different pain generating mechanisms, which may be utilized in designing new therapeutic drugs.

Original language	English
Journal	Pharmacology, Biochemistry and Behavior
Volume	91
Issue number	1
Pages (from-to)	38-46
Number of pages	9
ISSN	0091-3057
DOIs	https://doi.org/10.1016/j.pbb.2008.04.021
Publication status	Published - 2008

Keywords

Former Faculty of Pharmaceutical Sciences

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.pbb.2008.04.021

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Hald, A., Ding, M., Egerod, K. L., Hansen, R. R., Konradsen, D., Jørgensen, S. G., Atalay, B., Nasser, A., Bjerrum, O. J., & Heegaard, A.-M. (2008). Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain. Pharmacology, Biochemistry and Behavior, 91(1), 38-46. https://doi.org/10.1016/j.pbb.2008.04.021

Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain. / Hald, Andreas; Ding, Ming; Egerod, Kristoffer Lihme et al.
In: Pharmacology, Biochemistry and Behavior, Vol. 91, No. 1, 2008, p. 38-46.

Research output: Contribution to journal › Journal article › Research › peer-review

Hald, A, Ding, M, Egerod, KL , Hansen, RR, Konradsen, D, Jørgensen, SG, Atalay, B, Nasser, A, Bjerrum, OJ & Heegaard, A-M 2008, 'Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain', Pharmacology, Biochemistry and Behavior, vol. 91, no. 1, pp. 38-46. https://doi.org/10.1016/j.pbb.2008.04.021

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abstract = "Pain due to bone malignancies is one of the most difficult types of cancer pain to fully control and may further decrease the patients' quality of life. Animal models of chronic pain conditions resulting from peripheral inflammatory reactions or nerve injuries are responsive to treatment with cannabinoid agonists. However, the use of cannabinoid agonists in humans may be hampered by CNS related side effects and development of tolerance. In the present study, we investigated the effect of repeated low dose administration of the synthetic cannabinoid agonist WIN 55,212-2 on bone cancer pain and neuropathic pain in mice. In addition, we investigated the development of CNS related side effects and tolerance. We found that 0.5 mg/kg/day for 18 days reduced pain related behavior and expression of spinal glial fibrillary acidic protein in the bone cancer pain model but not in the neuropathic pain model. Furthermore, this treatment strategy was not found to induce measurable CNS related side effects or tolerance. Cancer cell viability assays and bone volume fraction assessed by micro computed tomography (microCT) demonstrated that these effects were not due to changes in cancer progression. The difference in WIN 55,212-2 efficacy between the bone cancer and neuropathic pain models may reflect the different pain generating mechanisms, which may be utilized in designing new therapeutic drugs.",

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AU - Hansen, Rikke Rie

AU - Konradsen, Dorthe

AU - Jørgensen, Stine G.

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AU - Bjerrum, Ole Jannik

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AB - Pain due to bone malignancies is one of the most difficult types of cancer pain to fully control and may further decrease the patients' quality of life. Animal models of chronic pain conditions resulting from peripheral inflammatory reactions or nerve injuries are responsive to treatment with cannabinoid agonists. However, the use of cannabinoid agonists in humans may be hampered by CNS related side effects and development of tolerance. In the present study, we investigated the effect of repeated low dose administration of the synthetic cannabinoid agonist WIN 55,212-2 on bone cancer pain and neuropathic pain in mice. In addition, we investigated the development of CNS related side effects and tolerance. We found that 0.5 mg/kg/day for 18 days reduced pain related behavior and expression of spinal glial fibrillary acidic protein in the bone cancer pain model but not in the neuropathic pain model. Furthermore, this treatment strategy was not found to induce measurable CNS related side effects or tolerance. Cancer cell viability assays and bone volume fraction assessed by micro computed tomography (microCT) demonstrated that these effects were not due to changes in cancer progression. The difference in WIN 55,212-2 efficacy between the bone cancer and neuropathic pain models may reflect the different pain generating mechanisms, which may be utilized in designing new therapeutic drugs.

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Differential effects of repeated low dose treatment with the cannabinoid agonist WIN 55,212-2 in experimental models of bone cancer pain and neuropathic pain

Abstract

Keywords

UN SDGs

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