Cannabimimetic activity, binding, and degradation of stearoylethanolamide within the mouse central nervous system.

Abstract

Stearoylethanolamide (SEA) is present in human, rat, and mouse brain in amounts comparable to those of the endocannabinoid anandamide (arachidonoylethanolamide, AEA). Yet, the biological activity of SEA has never been investigated. We report that SEA has the same effects as AEA on catalepsy, motility, analgesia, and body temperature of mice and that specific binding sites for SEA are present in mouse brain and are most abundant in cortex. Pharmacological experiments and the use of knockout mice demonstrated that these sites are different from cannabinoid receptors, are not coupled to G proteins, and regulate different signaling pathways. Mouse brain has also a specific SEA membrane transporter and a fatty acid amide hydrolase able to cleave SEA, with the same regional distribution as the binding sites of this lipid. Moreover, SEA potentiates the decrease of cAMP induced by AEA in mouse cortical slices, suggesting that SEA might also be an "entourage" compound.

• Authors: Mauro Maccarrone, Antonella Cartoni, Daniela Parolaro, Andrea Margonelli, Paola Massi, Monica Bari, Natalia Battista, Alessandro Finazzi-Agrò
• Journal: Molecular and cellular neurosciences (Mol Cell Neurosci) Vol. 21 Issue 1 Pg. 126-40 (Sep 2002) ISSN: 1044-7431 [Print] United States
• PMID: 12359156 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cannabinoid Receptor Modulators
• Cannabinoids
• Receptors, Cannabinoid
• Receptors, Drug
• Stearic Acids
• stearoylethanolamide

Topics

• Animals
• Binding Sites (physiology)
• Cannabinoid Receptor Modulators
• Cannabinoids (metabolism)
• Catalepsy (metabolism, physiopathology)
• Cerebral Cortex (metabolism)
• Hydrolysis
• Male
• Mice
• Protein Binding (physiology)
• Receptors, Cannabinoid
• Receptors, Drug (agonists, metabolism)
• Signal Transduction (physiology)
• Stearic Acids (metabolism)