Dual regulation by μ, δ and κ opioid receptor agonists of K+ conductance of DRG neurons and neuroblastoma × DRG neuron hybrid F11 cells
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Cited by (33)
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2010, Progress in NeurobiologyExcitatory and inhibitory effects of opioid agonists on respiratory motor output produced by isolated brainstems from adult turtles (Trachemys)
2010, Respiratory Physiology and NeurobiologyChapter 12 Functional genomics of sex hormone-dependent neuroendocrine systems: specific and generalized actions in the CNS
2006, Progress in Brain ResearchCitation Excerpt :The same mechanism stimulates G-protein-activated K+ conductance and phospholipase (Standifer and Pasternak, 1997; Quock et al., 1999). The biphasic nature of DPDPE was observed in DRG neurons and neuroblastoma×DRG neuron hybrid F11 cells for K+ conductance: at concentrations of <1 nM, conductance was inhibited (Fan et al., 1991), but at higher concentrations, conductance was increased (Fan and Crain, 1995). Like some other GPCRs, MORs, and DORs can express basal levels of constitutive activity and can activate G proteins in the absence of agonists.
Opioids and central sensitisation: II. Induction and reversal of hyperalgesia
2005, European Journal of PainNeuraminidase inhibitor, oseltamivir blocks GM1 ganglioside-regulated excitatory opioid receptor-mediated hyperalgesia, enhances opioid analgesia and attenuates tolerance in mice
2004, Brain ResearchCitation Excerpt :Our previous work has attributed these anti-analgesic tolerance effects of chronic opioid administration, as well as the hyperalgesia induced by acute, very low-dose morphine, to the efficacy of GM1-regulated excitatory signaling by Gs-coupled opioid receptors in nociceptive neurons [2,5–9]. Endogenous GM1 levels are significantly elevated by chronic opioid treatment of neuroblastoma×DRG neuron hybrid F-11 cells [34] (see also Ref. [11]), a finding that adds support to the hypothesis that oseltamivir blocks chronic morphine-induced hyperalgesia and tolerance by decreasing GM1 levels in nociceptive neurons. In vitro application of a specific neuraminidase inhibitor has previously been shown to decrease GM1 levels in the plasma membrane of neuroblastoma cells, indicated by a decrease in the binding of 125I-labeled CTX-B [38].