ArticleBritish journal of pharmacology2004
Agonist-dependence of recovery from desensitization of P2X(3) receptors provides a novel and sensitive approach for their rapid up or downregulation.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Investigation on 2',3'-ACS medicinal chemistry letters · 2019Article
- Anticancer, antimicrobial, and analgesic activities of spider venoms.Toxicology research · 2018Review
- 2',3'-O-Substituted ATP derivatives as potent antagonists of purinergic P2X3 receptors and potential analgesic agents.Purinergic signalling · 2017Article
- Nucleotide homeostasis and purinergic nociceptive signaling in rat meninges in migraine-like conditions.Purinergic signalling · 2016Article
- Stable, synthetic analogs of diadenosine tetraphosphate inhibit rat and human P2X3 receptors and inflammatory pain.Molecular pain · 2016Article
- Article
- Desensitization properties of P2X3 receptors shaping pain signaling.Frontiers in cellular neuroscience · 2013Review
- P2X3 receptor expression by HEK cells conditions their survival.Purinergic signalling · 2012Article
- Lipid rafts control P2X3 receptor distribution and function in trigeminal sensory neurons of a transgenic migraine mouse model.Molecular pain · 2011Article
- Amino acid residues constituting the agonist binding site of the human P2X3 receptor.The Journal of biological chemistry · 2011Article
- Familial hemiplegic migraine Ca(v)2.1 channel mutation R192Q enhances ATP-gated P2X3 receptor activity of mouse sensory ganglion neurons mediating trigeminal pain.Molecular pain · 2010Article
- Cutaneous sensory neurons expressing the Mrgprd receptor sense extracellular ATP and are putative nociceptors.Journal of neurophysiology · 2008Article
- Molecular mechanisms of sensitization of pain-transducing P2X3 receptors by the migraine mediators CGRP and NGF.Molecular neurobiology · 2008Review
- Neutralization of nerve growth factor induces plasticity of ATP-sensitive P2X3 receptors of nociceptive trigeminal ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Metabotropic P2Y receptors inhibit P2X3 receptor-channels via G protein-dependent facilitation of their desensitization.British journal of pharmacology · 2007Article
- Molecular properties of P2X receptors.Pflugers Archiv : European journal of physiology · 2006Review
- Delayed upregulation of ATP P2X3 receptors of trigeminal sensory neurons by calcitonin gene-related peptide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Desensitization of neuronal nicotinic receptors of human neuroblastoma SH-SY5Y cells during short or long exposure to nicotine.British journal of pharmacology · 2005Article
- Use-dependent inhibition of P2X3 receptors by nanomolar agonist.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Quantal release of ATP from clusters of PC12 cells.The Journal of physiology · 2004Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Fast-desensitizing P2X(3) receptors of nociceptive dorsol root ganglion (DRG) neurons are thought to mediate pain sensation. Since P2X(3) receptor efficiency is powerfully modulated by desensitization, its underlying properties were studied with patch-clamp recording. 2. On rat cultured DRG neurons, 2 s application of ATP (EC(50)=1.52 microm), ADP (EC(50)=1.1 microm) or alpha,beta-meATP (EC(50)=1.78 microm) produced similar inward currents that fully desensitized, at the same rate, back to baseline. Recovery from desensitization was much slower after ATP and ADP than after alpha,beta-meATP and, in all cases, it had sigmoidal time course. 3. By alternating the application of ATP and alpha,beta-meATP, we observed complete cross-desensitization indicating that these agonists activated the same receptors. This notion was confirmed by the similar antagonism induced by 2', 3'-O-(2,4,6,trinitrophenyl)-adenosine triphosphate (TNP-ATP). 4. Recovery from desensitization elicited by ATP was unexpectedly shaped by transient application of alpha,beta-methylene-adenosine triphosphate (alpha,beta-meATP), and vice versa. Thus, short-lasting, full desensitization produced by alpha,beta-meATP protected receptors from long-lasting desensitization induced by subsequent ATP applications. ATP and ADP had similar properties of recovery from desensitization. 5. Low nm concentrations of alpha,beta-meATP (unable to evoke membrane currents) could speed up recovery from ATP-induced desensitization, while low nm concentrations of ATP enhanced it. Ambient ATP levels were found to be in the pm range (52+/-3 pm). 6. The phenomenon of cross-desensitization and protection was reproduced by rP2X(3) receptors expressed by rat osteoblastic cell 17/2.8 or human embryonic kidney cell 293 cells, indicating P2X(3) receptor specificity. 7. It is suggested that transient application of an agonist that generates rapid recovery from desensitization, is a novel, powerful tool to modulate P2X(3) receptor responsiveness to the natural agonist ATP.
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