Abstract
Mu opioid receptors mediate positive reinforcement following direct (morphine) or indirect (alcohol, cannabinoids, nicotine) activation, and our understanding of mu receptor function is central to the development of addiction therapies. Recent data obtained in native neurons confirm that mu receptor signaling and regulation are strongly agonist-dependent. Current functional mapping reveals morphine-activated neurons in the extended amygdala and early genomic approaches have identified novel mu receptor-associated proteins. A classification of about 30 genes either promoting or counteracting the addictive properties of morphine is proposed from the analysis of knockout mice data. The targeting of effectors or regulatory proteins, beyond the mu receptor itself, might provide valuable strategies to treat addictive disorders.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Brain / drug effects*
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Brain / metabolism
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Brain / physiopathology
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / genetics
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Humans
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Morphine / pharmacology
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Narcotics / pharmacology*
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Nerve Tissue Proteins / biosynthesis
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Nerve Tissue Proteins / drug effects
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Neural Pathways / drug effects
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Neural Pathways / metabolism
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Neural Pathways / physiopathology
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Receptors, Opioid, mu / drug effects*
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Receptors, Opioid, mu / genetics
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Receptors, Opioid, mu / metabolism
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Signal Transduction / drug effects
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Signal Transduction / genetics
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Substance-Related Disorders / genetics*
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Substance-Related Disorders / metabolism*
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Substance-Related Disorders / therapy
Substances
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Narcotics
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Nerve Tissue Proteins
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Receptors, Opioid, mu
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Morphine