Biosynthesis of an endogenous cannabinoid precursor in neurons and its control by calcium and cAMP

Détails

ID Serval
serval:BIB_C3B63F3CA0A3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Biosynthesis of an endogenous cannabinoid precursor in neurons and its control by calcium and cAMP
Périodique
J Neurosci
Auteur(s)
Cadas H., Gaillet S., Beltramo M., Venance L., Piomelli D.
ISSN
0270-6474 (Print)
ISSN-L
0270-6474
Statut éditorial
Publié
Date de publication
1996
Peer-reviewed
Oui
Volume
16
Numéro
12
Pages
3934-42
Langue
anglais
Notes
Cadas, H
Gaillet, S
Beltramo, M
Venance, L
Piomelli, D
eng
J Neurosci. 1996 Jun 15;16(12):3934-42.
Résumé
Understanding the mechanisms involved in the biogenesis of N-arachidonoylethanolamine (anandamide) and N-palmitoylethanolamine is important in view of the possible role of these lipids as endogenous cannabinoid substances. Anandamide (which activates cannabinoid CB1 receptors) and N-palmitoylethanolamine (which activates a CB2-like receptor subtype in mast cells) may both derive from cleavage of precursor phospholipid, N-acylphosphatidylethanolamine (NAPE), catalyzed by Ca(2+)-activated D-type phosphodiesterase activity. We report here that the de novo biosynthesis of NAPE is enhanced in a Ca(2+)-dependent manner when rat cortical neurons are stimulated with the Ca(2+)-ionophore ionomycin or with membrane-depolarizing agents such as veratridine and kainate. This reaction is likely to be mediated by a neuronal N-acyltransferase activity, which catalyzes the transfer of an acyl group from phosphatidylcholine to the ethanolamine moiety of phosphatidylethanolamine. In addition, we show that Ca2+-dependent NAPE biosynthesis is potentiated by agents that increase cAMP levels, including forskolin and vasoactive intestinal peptide. Our results thus indicate that NAPE levels in cortical neurons are controlled by Ca2+ ions and cAMP. Such regulatory effect may participate in maintaining a supply of cannabimimetic N-acylethanolamines during synaptic activity, and prime target neurons for release of these bioactive lipids.
Mots-clé
Animals, Anti-Inflammatory Agents, Non-Steroidal/pharmacology, Arachidonic Acids/pharmacology, Arylamine N-Acetyltransferase/metabolism, Astrocytes/metabolism, Calcium/*pharmacology, Calcium Channel Blockers/pharmacology, Calmodulin/antagonists & inhibitors, Cannabinoids/*biosynthesis, Carbachol/pharmacology, Cyclic AMP/*metabolism, Endocannabinoids, Enzyme Inhibitors/pharmacology, Ethanolamine, Ethanolamines/metabolism, Imidazoles/pharmacology, Ionomycin/pharmacology, Ionophores/pharmacology, Neurons/*enzymology, Nicotinic Agonists/pharmacology, Palmitic Acids/pharmacology, Phosphatidylethanolamines/biosynthesis, Polyunsaturated Alkamides, Rats, Sodium Channel Agonists, Tritium/metabolism, Vasoactive Intestinal Peptide/pharmacology, Veratridine/pharmacology
Pubmed
Création de la notice
13/11/2017 10:57
Dernière modification de la notice
11/08/2018 6:26
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