ArticleJournal of neurochemistry2009
Supraspinal Gbetagamma-dependent stimulation of PLCbeta originating from G inhibitory protein-mu opioid receptor-coupling is necessary for morphine induced acute hyperalgesia.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Biasing G protein βγ subunit downstream signaling enhances the analgesic effects of endogenous opioid receptor agonists during nitroglycerin-induced thermal hypersensitivity.Molecular pharmacology · 2025Article
- Divergent gene expression patterns in alcohol and opioid use disorders lead to consistent alterations in functional networks within the dorsolateral prefrontal cortex.Translational psychiatry · 2024Article
- Biasing GMolecular pharmacology · 2024Article
- Divergent gene expression patterns in alcohol and opioid use disorders lead to consistent alterations in functional networks within the Dorsolateral Prefrontal Cortex.bioRxiv : the preprint server for biology · 2024Article
- Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach.Brain : a journal of neurology · 2023Review
- Coincident Regulation of PLCMolecular pharmacology · 2022Article
- Activation of Phospholipase C β by Gβγ and GαStructure (London, England : 1993) · 2020Article
- Targeting G protein-coupled receptor signalling by blocking G proteins.Nature reviews. Drug discovery · 2018Review
- Stress activates pronociceptive endogenous opioid signalling in DRG neurons during chronic colitis.Gut · 2017Article
- Molecular mechanisms of phospholipase C β3 autoinhibition.Structure (London, England : 1993) · 2014Article
- Structural insights into phospholipase C-β function.Molecular pharmacology · 2013Review
- Understanding molecular recognition by G protein βγ subunits on the path to pharmacological targeting.Molecular pharmacology · 2011Review
- Direct-reversible binding of small molecules to G protein βγ subunits.Biochimica et biophysica acta · 2011Article
- TRPA1 is required for histamine-independent, Mas-related G protein-coupled receptor-mediated itch.Nature neuroscience · 2011Article
- Mice lacking rhes show altered morphine analgesia, tolerance, and dependence.Neuroscience letters · 2011Article
- Tramadol-induced seizurogenic effect: a possible role of opioid-dependent histamine H1 receptor activation-linked mechanism.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
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Abstract
Although alterations in micro-opioid receptor (microOR) signaling mediate excitatory effects of opiates in opioid tolerance, the molecular mechanism for the excitatory effect of acute low dose morphine, as it relates to microOR coupling, is presently unknown. A pronounced coupling of microOR to the alpha subunit of G inhibitory protein emerged in periaqueductal gray (PAG) from mice systemically administered with morphine at a dose producing acute thermal hyperalgesia. This coupling was abolished in presence of the selective microOR antagonist d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH(2) administered at the PAG site, showing that the low dose morphine effect is triggered by microOR activated G inhibitory protein at supraspinal level. When Gbetagamma downstream signalling was blocked by intra-PAG co-administration of 2-(3,4,5-trihydroxy-6-oxoxanthen-9-yl)cyclohexane-1-carboxylic acid, a compound that inhibits Gbetagamma dimer-dependent signaling, a complete prevention of low dose morphine induced acute thermal hyperalgesia was obtained. Phospholipase C beta3, an enzyme necessary to morphine hyperalgesia, was revealed to be associated with Gbetagamma in PAG. Although opioid administration induces a shift in microOR-G protein coupling from Gi to Gs after chronic administration, our data support that this condition is not realized in acute treatment providing evidence that a separate molecular mechanism underlies morphine induced acute excitatory effect.
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