Document Detail


TRPV1: on the road to pain relief.
MedLine Citation:
PMID:  20021438     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Historically, drug research targeted to pain treatment has focused on trying to prevent the propagation of action potentials in the periphery from reaching the brain rather than pinpointing the molecular basis underlying the initial detection of the nociceptive stimulus: the receptor itself. This has now changed, given that many receptors of nociceptive stimuli have been identified and/or cloned. Transient Receptor Potential (TRP) channels have been implicated in several physiological processes such as mechanical, chemical and thermal stimuli detection. Ten years after the cloning of TRPV1, compelling data has been gathered on the role of this channel in inflammatory and neuropathic states. TRPV1 activation in nociceptive neurons, where it is normally expressed, triggers the release of neuropeptides and transmitters resulting in the generation of action potentials that will be sent to higher CNS areas where they will often be perceived as pain. Its activation also will evoke the peripheral release of pro-inflammatory compounds that may sensitize other neurons to physical, thermal or chemical stimuli. For these reasons as well as because its continuous activation causes analgesia, TRPV1 has become a viable drug target for clinical use in the management of pain. This review will provide a general picture of the physiological and pathophysiological roles of the TRPV1 channel and of its structural, pharmacological and biophysical properties. Finally, it will provide the reader with an overall view of the status of the discovery of potential therapeutic agents for the management of chronic and neuropathic pain.
Authors:
Andrés Jara-Oseguera; Sidney A Simon; Tamara Rosenbaum
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current molecular pharmacology     Volume:  1     ISSN:  1874-4702     ISO Abbreviation:  Curr Mol Pharmacol     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2009-12-21     Completed Date:  2010-02-24     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  101467997     Medline TA:  Curr Mol Pharmacol     Country:  United Arab Emirates    
Other Details:
Languages:  eng     Pagination:  255-69     Citation Subset:  IM    
Affiliation:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials
Antipruritics / chemistry,  pharmacology
Humans
Pain / drug therapy*
TRPV Cation Channels / antagonists & inhibitors*,  metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
DC-01065/DC/NIDCD NIH HHS; GM27278/GM/NIGMS NIH HHS; R01 DC001065-14A2/DC/NIDCD NIH HHS; R01 DC001065-15/DC/NIDCD NIH HHS; R01 DC001065-16/DC/NIDCD NIH HHS; R01 DC001065-17/DC/NIDCD NIH HHS
Chemical
Reg. No./Substance:
0/Antipruritics; 0/TRPV Cation Channels; 0/TRPV1 protein, human
Comments/Corrections

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