Redistribution of mu-opioid receptors in C1 adrenergic neurons following chronic administration of morphine

Drake, Carrie T.; Aicher, Sue A.; Montalmant, F.; Milner, Teresa A.

doi:10.1016/j.expneurol.2005.08.012

Cited by 17 publications

(18 citation statements)

References 32 publications

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“…Haberstock-Debic et al (2003) reported that in the rat nucleus accumbens, morphine (30 min) translocated MOPR to intracellular sites in dendrites, but not in neuronal cell bodies or axons. Drake et al (2005) also observed that, in the rostral ventrolateral medulla, morphine induced internalization of MOPR in dendrites that had diameters <.4 µm, but not in larger dendrites. These findings imply that the abundance of molecules involved in internalization machinery may vary in different compartments of neurons.…”

Section: Trafficking Of Opioid Receptors In Vivomentioning

confidence: 74%

“…Drake et al(2005) reported the majority of MOPR was located intracellularly in the dendrites of C1 adrenergic neurons in the rat rostral ventrolateral medulla, in contrast to other brain regions. Therefore, the differences in in vivo milieu, such as interacting proteins involved in trafficking, may lead to their differential subcellular distribution in brain regions.…”

Section: Future Studiesmentioning

confidence: 96%

“…In the dorsal horn of rat spinal cord, most of the peroxidase-labeled MOPR was associated with postsynaptic membranes of dendrites (Wang et al 2003). Surprisingly, the majority of immunogold-labeled MOPR (> 70%) was found in cytoplasm of the dendrites of C1 adrenergic neurons in the rat rostral ventrolateral medulla (Drake et al 2005). It may reflect the differential subcellular distribution of MOPR in brain regions.…”

Section: Differential Subcellular Localization Of Endogenous Opioid Rmentioning

confidence: 99%

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In vivo trafficking of endogenous opioid receptors

2008

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Several approaches have been taken for these in vivo studies. In many studies, the use of semiquantitative immuno-electron microscopy is the approach of choice. Endogenous opioid receptors display differential subcellular distributions with µ opioid receptor (MOPR) being mostly present on the plasma membrane and δ-and κ-opioid receptors (DOPR and KOPR, respectively) having a significant intracellular pool. Etorphine and DAMGO cause endocytosis of the MOPR, but morphine does not, except in some dendrites. Interestingly, chronic inflammatory pain and morphine treatment promote trafficking of intracellular DOPR to the cell surface which may account for the enhanced antinociceptive effects of DOPR agonists. KOPR has been reported to be associated with secretory vesicles in the posterior pituitary and translocated to the cell surface upon salt loading along with the release of vasopressin. The study of endogenous opioid receptors using in vivo models has produced some interesting results that could not have been anticipated in vitro. In vivo studies, therefore, are essential to provide insight into the mechanisms underlying opioid receptor regulation.

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Section: Trafficking Of Opioid Receptors In Vivomentioning

confidence: 74%

Section: Future Studiesmentioning

confidence: 96%

Section: Differential Subcellular Localization Of Endogenous Opioid Rmentioning

confidence: 99%

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In vivo trafficking of endogenous opioid receptors

2008

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“…There are a limited number of studies in which the cellular distribution of MORs was examined at the electron microscopic level following the chronic morphine treatment. In the adrenergic neurons of the medulla, chronic treatment with morphine (3 Â 75 mg morphine pellets) resulted in a dramatic redistribution of MORs from the plasma membrane to intracellular compartments (Drake et al, 2005). This is an important observation that may be one explanation for the decrease in effector activation that has been reported in physiologic studies discussed above.…”

Section: A Desensitization and Tolerance Are Both Associated With Rementioning

confidence: 76%

Regulation ofµ-Opioid Receptors: Desensitization, Phosphorylation, Internalization, and Tolerance

et al. 2013

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“…Chronically Agonist-Treated Animals -Opioid receptor traffi cking in chronically morphinetreated animals has only been directly examined in one study [86] , although a relative increase in intracellular versus plasma membrane -opioid receptor immunoreactivity was found in brainstem neurons from morphinetreated rats [87] . In the study where traffi cking was examined there was a signifi cant reduction in DAMGO-mediated anti-nociception in the treated animals but no change in the amount of -opioid receptor internalization in response to DAMGO [86] .…”

Section: -Opioid Receptor-traffi Cking Changes Inmentioning

confidence: 99%

The Role of Opioid Receptor Phosphorylation and Trafficking in Adaptations to Persistent Opioid Treatment

2005

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µ-Opioid receptor activation underpins clinical analgesia and is the central event in the abuse of narcotics. Continued opioid use produces tolerance to the acute effects of the drug and adaptations that lead to physical and psychological dependence. Continued µ-receptor signaling provides the engine for these adaptations, with most evidence suggesting that chronic agonist treatment produces only limited alterations in primary µ-opioid receptor signaling. Here we examine agonist regulation of µ-opioid receptor function, and whether this is altered by chronic treatment. Receptor phosphorylation is thought to be the key initial event in agonist regulation of the µ-opioid receptor, providing a signal for acute receptor desensitization and also subsequent receptor resensitization. Morphine appears to produce qualitatively and quantitatively different µ-receptor phosphorylation than other agonists, but the consequences of this remain obscure, at least in neurons. There is no evidence that agonist-induced µ-opioid receptor phosphorylation changes in chronically morphine-treated animals, although receptor regulation appears to be altered. Thus, as receptor phosphorylation and resensitization appear to maintain continued signaling through the µ-opioid receptor, these two events are crucial in facilitating adaptations to chronic opioid treatment, and the possibility that agonist-specific phosphorylation can contribute to the development of different adaptations remains open.

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Redistribution of mu-opioid receptors in C1 adrenergic neurons following chronic administration of morphine

Cited by 17 publications

References 32 publications

In vivo trafficking of endogenous opioid receptors

In vivo trafficking of endogenous opioid receptors

Regulation ofµ-Opioid Receptors: Desensitization, Phosphorylation, Internalization, and Tolerance

The Role of Opioid Receptor Phosphorylation and Trafficking in Adaptations to Persistent Opioid Treatment

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