Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture
Reference (70)
- et al.
Pertussis toxin blocks the outward currents evoked by opiate and alpha2-agonists in locus coeruleus neurons
Brain Research
(1986) - et al.
Common alpha2- and opiate effector mechanisms in the locus coeruleus: intracellular studies in brain slices
Neuropharmacology
(1987) - et al.
Maturation of opioid sensitivity of fetal mouse dorsal-root ganglion neuron perikarya in organotypic cultures: regulation by spinal cord
Neuroscience
(1986) - et al.
Inhibitor of cyclic AMP-dependent protein kinase blocks opioid-induced prolongation of the action potential of mouse sensory ganglion neurons in dissociated cell cultures
Brain Research
(1988) - et al.
Pertussis toxin blocks depressant effect of opioid, monoaminergic and muscarinic agonists on dorsal-horn network responses in spinal cord-ganglion cultures
Brain Research
(1987) - et al.
Cyclic AMP or forskolin rapidly attenuates the depressant effect of opioids on sensory-evoked dorsal-horn responses in mouse spinal cord-ganglion explants
Brain Research
(1986) - et al.
Opioids excite rather than inhibit sensory neurons after chronic opioid exposure of spinal cord-ganglion cultures
Brain Research
(1988) - et al.
Opioid receptor subtypes in the rat spinal cord: electrophysiological studies with mu- and delta-opioid receptor agonists in the control of nociception
Brain Research
(1987) Nucleotide binding proteins in signal transduction and disease
Trends Neurosci.
(1987)- et al.
G proteins as regulators of ion channel function
Trends Neurosci.
(1987)
G proteins and dual control of adenylate cyclase
Cell
(1984)
Receptor regulated G proteins
Trends Neurosci.
(1986)
Analogues of beta-LPH 61–64 possessing selective agonist activity at mu-opiate receptors
Eur. J. Pharmacol.
(1981)
Morphine enhances and depresses Ca2+-dependent responses in visceral primary afferent neurons
Brain Research
(1982)
Chemoreceptors for serotonin, acetylcholine, bradykinin, histamine and gamma-aminobutyric acid on rabbit visceral afferent receptors
Brain Res. Bull.
(1982)
Mechanisms of receptor-mediated modulation of transmitter release in noradrenergic, cholinergic and sensory neurones
Neuroscience
(1986)
Paradoxical hyperalgesic effect of exceedingly low doses of systemic morphine in an animal model of persistent pain (Freund's adjuvant-induced arthritis rats)
Brain Research
(1987)
Effects of selective and non-selective kappa-opioid receptor agonists on cutaneous C-fibre-evoked responses of rat dorsal horn neurones
Brain Research
(1987)
Specific uncoupling by islet-activating protein,pertussis toxin, of negative signal transduction via alpha-adrenergic, cholinergic, and opiate receptors in neuroblastoma × glioma hybrid cells
J. Biol. Chem.
(1983)
Modulation of adenylate cyclase activity of mouse spinal cord-ganglion explants by opioids, serotonin andpertussis toxin
Brain Research
(1988)
Regulation of adenylate cyclase of neuroblastoma × glioma hybrid cells by alpha-adrenergic receptor. I. Inhibition of adenylate cyclase mediated by alpha-receptors
J. Biol. Chem.
(1979)
Nucleotides such as ATP may control the activity of ion channels
Trends Neurosci.
(1987)
Hyperalgesia mediated by peripheral opiate receptors in the rat
Behav. Brain Res.
(1985)
Bradykinin inhibits a slow spike afterhyperpolarization in visceral sensory neurons
Eur. J. Pharmacol.
(1986)
Opioid peptides decrease calcium-dependent action potential duration of mouse dorsal root ganglion neurons in cell culture
Brain Research
(1982)
Opioid peptides selective for mu- and delta-opiate receptors reduce calcium-dependent action potential duration by increasing potassium conductance
Neurosci. Lett.
(1983)
Corticotropin releasing factor decreases postburst hyperpolarizations and excites hippocampal neurons
Science
(1983)
Adenosine 5′-triphosphate-sensitive potassium channels
Annu. Rev. Neurosci.
(1988)
Inhibitor of adenosine 3′:5′-monophosphate-dependent protein kinase blocks presynaptic facilitation inAplysia
J. Neurosci.
(1982)
Sufentanil, κ-agonist U50,488H andd-Ala2-Met5-enkephalinamide inhibit substance P release from primary sensory neurons
Soc. Neurosci. Abstr.
(1988)
μ and κ opioids inhibit transmitter release by different mechanisms
Cellular site of opiate dependence
Nature (Lond.)
(1980)
Regulation of excitatory opioid responsivity of dorsal root ganglion neurons
Electrophysiologic responses and adenylate cyclase activities of mouse spinal cord-dorsal root ganglion explants rendered tolerant by chronic exposure to morphine orpertussis toxin
Altered pharmacologic responsivity of opioid-sensitive dorsal root ganglion (DRG) neurons rendered hyperexcitable by exposure of DRG-cord explants to forskolin or pertussis toxin
Cited by (188)
Resveratrol protects bupivacaine-induced neuro-apoptosis in dorsal root ganglion neurons via activation on tropomyosin receptor kinase A
2018, Biomedicine and PharmacotherapyInhibition of spinal ERK1/2-c-JUN signaling pathway counteracts the development of low doses morphine-induced hyperalgesia
2015, European Journal of PharmacologyThe multi-tasked life of GM1 ganglioside, a true factotum of nature
2015, Trends in Biochemical SciencesActivation of Mas oncogene-related gene (Mrg) C receptors enhances morphine-induced analgesia through modulation of coupling of μ-opioid receptor to Gi-protein in rat spinal dorsal horn
2013, NeuroscienceCitation Excerpt :Despite tremendous efforts in the development of analgesics, μ-opiates are still the most powerful drugs for pain management. MORs are believed to be predominantly coupled to the pertussis toxin-sensitive Gi and Go proteins in normal condition (Chalecka-Franaszek et al., 2000) while only a small fraction of these receptors is coupled to Gs protein (Shen and Crain, 1989; Fan et al., 1991). However, repeated administration of morphine switches MOR coupled from Gi/o-protein to Gs-protein, leading to the decline of morphine analgesia (Wang et al., 2005).
Preliminary reports of this study have been published (see refs. 15, 54, 55).
Copyright © 1989 Published by Elsevier B.V.