Absence of μ opioid receptor mRNA expression in astrocytes and microglia of rat spinal cord.

Neuroreport
Sheng-Chin KaoYuan-Xiang Tao

Abstract

Cumulating evidence has demonstrated that μ opioid receptor (MOR) agonists promote spinal glial activation, lead to synthesis and release of proinflammatory cytokines and chemokines, and contribute to opioid-induced hyperalgesia and development of opioid tolerance and dependence. However, whether these MOR agonists directly or indirectly act on spinal cord astrocytes and microglial cells in vivo is unclear. In the present study, by combining the techniques of in-situ hybridization of MOR mRNA with immunohistochemistry of glial fibrillary acidic protein (GFAP; an astrocyte marker) and Iba1 (a microglial marker), we examined expression and distribution of GFAP, Iba1, and MOR mRNA in the spinal cord of rats under chronic morphine tolerance conditions. Intrathecal injections of morphine twice daily for 7 days reduced morphine analgesic effect and increased both GFAP and Iba1 immunostaining densities in the spinal cord. Surprisingly, neither GFAP nor Iba1 colocalized with MOR mRNA in spinal cord cells. Our findings indicate that MOR expression is absent from spinal cord astrocytes and microglia, suggesting that these cell types are indirectly activated by MOR agonists under chronic opioid tolerance conditions.

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Citations

Oct 16, 2013·Peptides·Richard J Bodnar
Feb 13, 2013·Pain Research and Treatment·Joel S Goldberg
Jan 3, 2014·The Journal of Clinical Investigation·Ji-Tian XuYuan-Xiang Tao
Dec 14, 2012·Expert Review of Neurotherapeutics·Jacob Thomas, Mark R Hutchinson
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Jan 22, 2019·Frontiers in Psychiatry·Tando MadunaClaire Gaveriaux-Ruff
Mar 21, 2020·Frontiers in Immunology·Halina Machelska, Melih Ö Celik
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