Direct evidence for activation and desensitization of the capsaicin receptor by N-oleoyldopamine on TRPV1-transfected cell, line in gene deleted mice and in the rat☆
Section snippets
Acknowledgements
This study was supported by Hungarian Grants OTKA T-034911, T-037523, TS-040753, ETT03-326/2003, NRDP1A/0021/2002, NRDP1/047/2001. G. Pethő was supported by the Bolyai János Research Fellowship. We are grateful to Dr John B. Davis, GlaxoSmithKline, Harlow, UK for providing the TRPV1 knockout mice.
References (18)
- et al.
N-Oleoyldopamine, a novel endogenous capsaicin-like lipid that produces hyperalgesia
J. Biol. Chem.
(2003) - et al.
The diversity in the vanilloid (TRPV) receptor family of ion channels
Trends Pharmacol. Sci.
(2002) - et al.
Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat
Life Sci.
(2003) - et al.
Concentration-dependent dual effect of anandamide on sensory neuropeptide release from isolated rat tracheae
Neurosci. Lett.
(2003) - et al.
Cannabinoid modulation of sensory neurotransmission via cannabinoid and vanilloid receptors: roles in regulation of cardiovascular function
Life Sci.
(2002) - et al.
Neonatal anandamide treatment results in prolonged mitochondrial damage in the vanilloid receptor type 1-immunoreactive B-type neurons of the rat trigeminal ganglion
Neuroscience
(2002) Anandamide and the question of its functional role for activation of capsaicin receptors
Trends Pharmacol. Sci.
(2000)- et al.
Arachidonyl dopamine as a ligand for the vanilloid receptor VR1 of the rat
Life Sci.
(2003) Ethical guidelines for investigations of experimental pain in conscious animals
Pain
(1983)
Cited by (25)
Lipids as central modulators of sensory TRP channels
2017, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :This lipid can activate TRPV1 through a binding site in the C-terminal domain of the channel, indicating a key role of this lipid in pain transduction [80]. AEA and related congeners oleoylethanolamide (OEA), N-arachidonoyl dopamine (NADA) and N-oleyl-dopamine (OLDA) all activate TRPV1 [81–85]. AEA acts as a full TRPV1 agonist in blood vessels and mesenteric arterial bed, provoking vasodilation through CGRP release, and as a partial agonist in the bronchus, DRG and trigeminal neurons, contributing to the development of respiratory disorders, pain and hyperalgesia [86].
N-Acyldopamines and N-Acylserotonins: From Synthetic Pharmacological Tools to Endogenous Multitarget Mediators
2015, The Endocannabinoidome: The World of Endocannabinoids and Related MediatorsEffects of single swim stress on changes in TRPV1-mediated plasticity in the amygdala
2013, Behavioural Brain ResearchAntinociceptive desensitizing actions of TRPV1 receptor agonists capsaicin, resiniferatoxin and N-oleoyldopamine as measured by determination of the noxious heat and cold thresholds in the rat
2010, European Journal of PainCitation Excerpt :The finding that the cold threshold returned to control level much earlier than the heat threshold also supports the view that noxious cold and heat responsiveness are mediated by at least partly different fiber populations. Previously we have shown that intraplantar injection of RTX or OLDA induces acute nocifensive behaviour and a marked decrease of the heat threshold interpreted as heat hyperalgesia (Almási et al., 2003; Szolcsányi et al., 2004). The present finding that these acute effects of either RTX or OLDA were almost abolished by i.pl.
The vanilloid receptor TRPV1: Role in cardiovascular and gastrointestinal protection
2010, European Journal of PharmacologyEffects of analgesics on the plantar incision-induced drop of the noxious heat threshold measured with an increasing-temperature water bath in the rat
2009, European Journal of Pharmacology
- ☆
This manuscript is in honor of Professor Manfred Zimmermann's 70th birthday.