Neuron
ArticleOpioid inhibition of Ih via adenylyl cyclase
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Immune cell-mediated opioid analgesia
2020, Immunology LettersCitation Excerpt :Through the Gαi/o-dependent inhibition of adenylyl cyclase, cyclic adenosine monophosphate formation and protein kinase A activity, mu-receptor agonists suppress several ion channels involved in pain facilitation. These channels include hyperpolarization-activated cyclic nucleotide-gated channels, voltage-gated Na+ channels, transient receptor potential cation channel subfamily V member 1 (TRPV1), and acid-sensing ion channels [43–47]. Additionally, mu-receptors mediate inhibition of purinergic 2X receptor-induced currents and action potential-evoked Ca2+ transients regulated by big conductance Ca2+-activated K+ channels [48,49].
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2018, Pharmacology and TherapeuticsPotential role of CXCL10/CXCR3 signaling in the development of morphine tolerance in periaqueductal gray
2017, NeuropeptidesCitation Excerpt :When morphine binds to mu opioid receptor (MOR), multiple intracellular downstream pathways could be activated. The Gα and Gβγ subunits dissociate from one another, which subsequently lead to the inhibition of cyclic-adenosine monophosphate (cAMP) formation and calcium conductance to produce the analgesic effect (Ingram and Williams, 1994; Schroeder et al., 1991). Previous study showed that inhibiting Gi protein could partially block the algesia induced by CXCL10, indicating that Gi protein is involved in the nociceptive signaling pathway related to CXCR3 (Ye et al., 2014).