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Molecular characterization of an enzyme that degrades neuromodulatory fatty-acid amides
TLDR
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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A Comprehensive Profile of Brain Enzymes that Hydrolyze the Endocannabinoid 2‐Arachidonoylglycerol
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Supersensitivity to anandamide and enhanced endogenous cannabinoid signaling in mice lacking fatty acid amide hydrolase
TLDR
Results indicate that FAAH is a key regulator of anandamide signaling in vivo, setting an endogenous cannabinoid tone that modulates pain perception, and may represent an attractive pharmaceutical target for the treatment of pain and neuropsychiatric disorders.
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Selective blockade of 2-arachidonoylglycerol hydrolysis produces cannabinoid behavioral effects
TLDR
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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Noxious compounds activate TRPA1 ion channels through covalent modification of cysteines
The nervous system senses peripheral damage through nociceptive neurons that transmit a pain signal. TRPA1 is a member of the Transient Receptor Potential (TRP) family of ion channels and is…
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Structure and function of fatty acid amide hydrolase.
TLDR
Investigations into the structure and function of FAAH have engendered provocative molecular models to explain how this enzyme integrates into cell membranes and terminates fatty acid amide signaling in vivo, as well as their biological and therapeutic implications.
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Endocannabinoid Hydrolysis Generates Brain Prostaglandins That Promote Neuroinflammation
TLDR
These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.
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Dual blockade of FAAH and MAGL identifies behavioral processes regulated by endocannabinoid crosstalk in vivo
TLDR
A selective and efficacious dual FAAH/MAGL inhibitor is described and it is shown that this agent exhibits broad activity in the tetrad test for CB1 agonism, causing analgesia, hypomotilty, and catalepsy, indicating that AEA and 2-AG signaling pathways interact to regulate specific behavioral processes in vivo, including those relevant to drug abuse.
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Chronic monoacylglycerol lipase blockade causes functional antagonism of the endocannabinoid system
TLDR
Individual endocannabinoids generate distinct analgesic profiles that are either sustained or transitory and associated with agonism and functional antagonism of the brain cannabinoid system, respectively.
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Characterization of monoacylglycerol lipase inhibition reveals differences in central and peripheral endocannabinoid metabolism.
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