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Open AccessJournal ArticleDOI

A Comprehensive Profile of Brain Enzymes that Hydrolyze the Endocannabinoid 2-Arachidonoylglycerol

TLDR
It is revealed that approximately 85% of brain 2-AG hydrolase activity can be ascribed to MAGL, and that the remaining 15% is mostly catalyzed by two uncharacterized enzymes, ABHD6 and ABHD12.
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This article is published in Chemistry & Biology.The article was published on 2007-12-26 and is currently open access. It has received 1031 citations till now. The article focuses on the topics: JZL195 & JZL184.

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Endocannabinoid-Mediated Control of Synaptic Transmission

TL;DR: This review aims to integrate the current understanding of functions of the endocannabinoid system, especially focusing on the control of synaptic transmission in the brain, and summarizes recent electrophysiological studies carried out on synapses of various brain regions and discusses how synaptic transmission is regulated by endoc cannabinoidoid signaling.
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Selective blockade of 2-arachidonoylglycerol hydrolysis produces cannabinoid behavioral effects

TL;DR: 2-AG endogenously modulates several behavioral processes classically associated with the pharmacology of cannabinoids and point to overlapping and unique functions for 2-AG and anandamide in vivo, indicating a functional segregation of endocannabinoid signaling pathways in vivo.
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Monoacylglycerol Lipase Regulates a Fatty Acid Network that Promotes Cancer Pathogenesis

TL;DR: Overexpression of MAGL in nonaggressive cancer cells recapitulates this fatty acid network and increases their pathogenicity-phenotypes that are reversed by an MAGL inhibitor, indicating that exogenous sources of fatty acids can contribute to malignancy in cancers lacking MAGL activity.
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Endocannabinoid Signaling and Synaptic Function

TL;DR: New advances in synaptic endocannabinoid signaling in the mammalian brain are focused on and the emerging picture not only reinforcesendocannabinoids as potent regulators of synaptic function but also reveals that endoc cannabinoidoid signaling is mechanistically more complex and diverse than originally thought.
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Targeting the endocannabinoid system: to enhance or reduce?

TL;DR: The discovery of compounds that either prolong the lifespan of endocannabinoids or tone down their action for the potential future treatment of pain, affective and neurodegenerative disorders, gastrointestinal inflammation, obesity and metabolic dysfunctions, cardiovascular conditions and liver diseases is discovered.
References
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Journal ArticleDOI

An approach to correlate tandem mass spectral data of peptides with amino acid sequences in a protein database.

TL;DR: The approach described in this manuscript provides a convenient method to interpret tandem mass spectra with known sequences in a protein database.
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Molecular characterization of an enzyme that degrades neuromodulatory fatty-acid amides

TL;DR: It is shown that oleamide hydrolase may serve as the general inactivating enzyme for a growing family of bioactive signalling molecules, the fatty-acid amides6–8, and the structure and sleep-inducing properties of cis-9-octadecenamide, a lipid isolated from the cerebrospinal fluid of sleep-deprived cats are reported.
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The molecular logic of endocannabinoid signalling

TL;DR: The endocannabinoids are a family of lipid messengers that engage the cell surface receptors that are targeted by Δ9-tetrahydrocannabinol, the active principle in marijuana (Cannabis).
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The endogenous cannabinoid system controls extinction of aversive memories

TL;DR: Treatment of wild-type mice with the CB1 antagonist SR141716A mimicked the phenotype of CB1-deficient mice, revealing that CB1 is required at the moment of memory extinction, and proposes that endocannabinoids facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala.
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Leptin-regulated endocannabinoids are involved in maintaining food intake

TL;DR: It is shown that following temporary food restriction, CB1 receptor knockout mice eat less than their wild-type littermates, and the CB1 antagonist SR141716A reduces food intake in wild- type but not knockout mice, which indicates that endocannabinoids in the hypothalamus may tonically activate CB1 receptors to maintain food intake and form part of the neural circuitry regulated by leptin.
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