Endogenous opiates and behavior: 2009

Bodnar, Richard J.

doi:10.1016/j.peptides.2010.09.016

Cited by 55 publications

(21 citation statements)

References 1,902 publications

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“…Numerous reports have examined how opioid signaling causes opioid-induced analgesia (For recent reviews see Bodnar 2010 (127) ; Walwyn et al, 2010 (3) ). It is generally accepted that MOR signaling to pertussis toxin sensitive Gαi is required for morphine antinociception.…”

Section: Opioid Signaling and Behaviormentioning

confidence: 99%

Molecular Mechanisms of Opioid Receptor-dependent Signaling and Behavior

2011

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Opioid receptors have been targeted for the treatment of pain and related disorders for thousands of years, and remain the most widely used analgesics in the clinic. Mu (μ), kappa (κ), and delta (δ) opioid receptors represent the originally classified receptor subtypes, with opioid receptor like-1 (ORL1) being the least characterized. All four receptors are G-protein coupled, and activate inhibitory G-proteins. These receptors form homo- and hetereodimeric complexes, signal to kinase cascades, and scaffold a variety of proteins. In this review, we discuss classical mechanisms and developments in understanding opioid tolerance, opioid receptor signaling, and highlight advances in opioid molecular pharmacology, behavioral pharmacology, and human genetics. We put into context how opioid receptor signaling leads to the modulation of behavior with the potential for therapeutic intervention. Finally, we conclude that there is a continued need for more translational work on opioid receptors in vivo.

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Section: Opioid Signaling and Behaviormentioning

confidence: 99%

Molecular Mechanisms of Opioid Receptor-dependent Signaling and Behavior

2011

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“…Delta (DOR) and Mu (MOR) opioid receptors belong to the G-protein couple receptors (GPCR) superfamily, and upon activation they regulate a variety of physiological functions inlcuding pain processing, anxiety, and reward (for review see (Bodnar, 2010)). Following activation, opioid receptors, like most GPCRs, can be rapidly phosphorylated by GPCR kinases (GRKs), bind arrestin proteins (Ferguson et al, 1998) and be endocytosed.…”

Section: Introductionmentioning

confidence: 99%

Heteromerization of the μ- and δ-Opioid Receptors Produces Ligand-Biased Antagonism and Alters μ-Receptor Trafficking

Milan‐Lobo

Whistler

2011

J Pharmacol Exp Ther

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Heteromerization of opioid receptors has been shown to alter opioid receptor pharmacology. However, how receptor heteromerization affects the processes of endocytosis and post-endocytic sorting has not been closely examined. This question is of particular relevance for heteromers of the mu and delta opioid receptor (MOR and DOR respectively), since the MOR is primarily recycled after endocytosis and the DOR is degraded in the lysosome. Here we examined the endocytic and post-endocytic fate of MORs, DORs and DOR/MOR heteromers in HEK293 stably expressing each receptor alone or co-expressing both receptors. We found that the clinically relevant MOR agonist methadone promotes endocytosis of MOR but also of the DOR/MOR heteromer. Furthermore, we show that DOR/MOR heteromers that are endocytosed in response to methadone are targeted for degradation, while MORs in the same cell are significantly more stable. Importantly, we found that the DOR-selective antagonist naltriben (NTB) could block both methadone- and DAMGO-induced endocytosis of the DOR/MOR heteromers but did not block signaling from this heteromer. Together, our results suggest that the MOR adopts novel trafficking properties in the context of the DOR/MOR heteromer. In addition, they suggest that the heteromer shows “biased antagonism”, whereby DOR antagonist can inhibit trafficking but not signaling of the DOR/MOR heteromer.

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“…Besides THC, approximately 100 other cannabinoids have been identified [21,22] including one of special scientific interest called "cannabidiol" (CBD) [23]. The human body produces both endogenous cannabinoids (endocannabinoids) and opioids (endorphins) and contains specific receptors for these substances [24,25]. There is an extensive literature on opioids but far less on cannabis/cannabinoids (CC).…”

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confidence: 99%

Prescribing cannabis for harm reduction

Collen¹

2012

Harm Reduction Journal

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Neuropathic pain affects between 5% and 10% of the US population and can be refractory to treatment. Opioids may be recommended as a second-line pharmacotherapy but have risks including overdose and death. Cannabis has been shown to be effective for treating nerve pain without the risk of fatal poisoning. The author suggests that physicians who treat neuropathic pain with opioids should evaluate their patients for a trial of cannabis and prescribe it when appropriate prior to using opioids. This harm reduction strategy may reduce the morbidity and mortality rates associated with prescription pain medications.

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Endogenous opiates and behavior: 2009

Cited by 55 publications

References 1,902 publications

Molecular Mechanisms of Opioid Receptor-dependent Signaling and Behavior

Molecular Mechanisms of Opioid Receptor-dependent Signaling and Behavior

Heteromerization of the μ- and δ-Opioid Receptors Produces Ligand-Biased Antagonism and Alters μ-Receptor Trafficking

Prescribing cannabis for harm reduction

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