Document Detail


Receptor-independent actions of cannabinoids on cell membranes: focus on endocannabinoids.
MedLine Citation:
PMID:  16584786     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cannabinoids are a structurally diverse group of mostly lipophilic molecules that bind to cannabinoid receptors. In fact, endogenous cannabinoids (endocannabinoids) are a class of signaling lipids consisting of amides and esters of long-chain polyunsaturated fatty acids. They are synthesized from lipid precursors in plasma membranes via Ca(2+) or G-protein-dependent processes and exhibit cannabinoid-like actions by binding to cannabinoid receptors. However, endocannabinoids can produce effects that are not mediated by these receptors. In pharmacologically relevant concentrations, endocannabinoids modulate the functional properties of voltage-gated ion channels including Ca(2+) channels, Na(+) channels, various types of K(+) channels, and ligand-gated ion channels such as serotonin type 3, nicotinic acetylcholine, and glycine receptors. In addition, modulatory effects of endocannabinoids on other ion-transporting membrane proteins such as transient potential receptor-class channels, gap junctions and transporters for neurotransmitters have also been demonstrated. Furthermore, functional properties of G-protein-coupled receptors for different types of neurotransmitters and neuropeptides are altered by direct actions of endocannabinoids. Although the mechanisms of these effects are currently not clear, it is likely that these direct actions of endocannabinoids are due to their lipophilic structures. These findings indicate that additional molecular targets for endocannabinoids exist and that these targets may represent novel sites for cannabinoids to alter either the excitability of the neurons or the response of the neuronal systems. This review focuses on the results of recent studies indicating that beyond their receptor-mediated effects, endocannabinoids alter the functions of ion channels and other integral membrane proteins directly.
Authors:
Murat Oz
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Publication Detail:
Type:  Journal Article; Review     Date:  2006-04-11
Journal Detail:
Title:  Pharmacology & therapeutics     Volume:  111     ISSN:  0163-7258     ISO Abbreviation:  Pharmacol. Ther.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-05-29     Completed Date:  2006-11-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905840     Medline TA:  Pharmacol Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  114-44     Citation Subset:  IM    
Affiliation:
National Institute on Drug Abuse, NIH/DHHS, Intramural Research Program, Cellular Neurobiology Branch, 5500 Nathan Shock Drive, Baltimore MD, 21224, USA. moz@intra.nida.nih.gov
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MeSH Terms
Descriptor/Qualifier:
Animals
Arachidonic Acid / metabolism
Cannabinoids / pharmacology
Cell Membrane / drug effects*,  physiology
Endocannabinoids / metabolism,  pharmacology*
Humans
Ion Channels / drug effects,  physiology
Ligands
Receptors, G-Protein-Coupled / drug effects,  physiology
Chemical
Reg. No./Substance:
0/Cannabinoids; 0/Endocannabinoids; 0/Ion Channels; 0/Ligands; 0/Receptors, G-Protein-Coupled; 506-32-1/Arachidonic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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