Nuclear factor κb signaling in opioid functions and receptor gene expression

Yulong L. Chen, Ping-Yee Law, Horace H Loh

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)270-279
Number of pages10
JournalJournal of Neuroimmune Pharmacology
Issue number3
StatePublished - Sep 2006

Bibliographical note

Funding Information:
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.


  • Akt
  • Gene expression
  • NF-κB
  • Opioid receptor
  • PI3K


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