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Nuclear Factor κB Signaling in Opioid Functions and Receptor Gene Expression

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Abstract

Opiates are the most powerful of all known analgesics. The prototype opiate morphine has been used as a painkiller for several thousand years. Chronic usage of opiates not only causes drug tolerance, dependence, and addiction, but also suppresses immune functions and affects cell proliferation and cell survival. The diverse functions of opiates underscore the complexity of opioid receptor signaling. Several downstream signaling effector systems, including adenylyl cyclase, mitogen-activated protein kinase, Ca2+ channels, K+ channels, and phosphatidylinositol 3-kinase/Akt, have been identified to be critical in opioid functions. Nuclear factor-κB (NF-κB), one of the most diverse and critical transcription factors, is one of the downstream molecules that may either directly or indirectly transmit the receptor-mediated upstream signals to the nucleus, resulting in the regulation of the NF-κB-dependent genes, which are critical for the opioid-induced biological responses of neuronal and immune cells. In this minireview, we focus on current understanding of the involvement of NF-κB signaling in opioid functions and receptor gene expression in cells.

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Acknowledgements

This work was supported by National Institute of Health Grants DA000564, DA001583, DA011806, DA007339, DA016674, K05-DA70554 (HHL), and K05-DA00513 (PYL), and by the A. & F. Stark Fund of the Minnesota Medical Foundation.

We apologize to many authors whose contributions could not be discussed or whose primary references could not be cited in this review due to space limitation. We also thank Susan Marriott for editorial assistance in preparation of the abstract of this revised manuscript.

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Chen, Y.L., Law, PY. & Loh, H.H. Nuclear Factor κB Signaling in Opioid Functions and Receptor Gene Expression. Jrnl Neuroimmune Pharm 1, 270–279 (2006). https://doi.org/10.1007/s11481-006-9028-0

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