We are analyzing https://link.springer.com/article/10.1385/mn:21:1-2:021.

Title:
Opioid tolerance and the emergence of new opioid receptor-coupled signaling | Molecular Neurobiology
Description:
Multiple cellular adaptations are elicited by chronic exposure to opioids. These include diminution of spare opioid receptors, decreased opioid receptor density, and G-protein content and coupling thereof. All imply that opioid tolerance is a manifestation of a loss of opioid function, i.e., desensitization. Recent observations challenge the exclusiveness of this formulation and indicate that opioid tolerance also results from qualitative changes in opioid signaling. In this article, Gintzler and Chakrabarti discuss the evidence that suggests that opioid tolerance results not only from impaired opioid receptor functionality, but also from altered consequences of coupling. Underlying the latter are fundamental changes in the nature of effectors that are coupled to the opioid receptor/G-protein signaling pathway. These molecular changes include the upregulation of adenylyl cyclase isoforms of the type II family as well as a substantial increase in their phosphorylation state. As a result, there is a shift in opioid receptor/G-protein signaling from predominantly Giα inhibitory to Gβγ stimulatory following chronic in vivo morphine exposure. These adaptations to chronic morphine indicate the plasticity of opioid-signal transduction mechanisms and the ability of chronic morphine to augment new signaling strategies.
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Keywords {🔍}

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Topics {✒️}

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         description:Multiple cellular adaptations are elicited by chronic exposure to opioids. These include diminution of spare opioid receptors, decreased opioid receptor density, and G-protein content and coupling thereof. All imply that opioid tolerance is a manifestation of a loss of opioid function, i.e., desensitization. Recent observations challenge the exclusiveness of this formulation and indicate that opioid tolerance also results from qualitative changes in opioid signaling. In this article, Gintzler and Chakrabarti discuss the evidence that suggests that opioid tolerance results not only from impaired opioid receptor functionality, but also from altered consequences of coupling. Underlying the latter are fundamental changes in the nature of effectors that are coupled to the opioid receptor/G-protein signaling pathway. These molecular changes include the upregulation of adenylyl cyclase isoforms of the type II family as well as a substantial increase in their phosphorylation state. As a result, there is a shift in opioid receptor/G-protein signaling from predominantly Giα inhibitory to Gβγ stimulatory following chronic in vivo morphine exposure. These adaptations to chronic morphine indicate the plasticity of opioid-signal transduction mechanisms and the ability of chronic morphine to augment new signaling strategies.
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      headline:Opioid tolerance and the emergence of new opioid receptor-coupled signaling
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