PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28193523-1 2017 Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear. aea 132-158 fatty acid amide hydrolase Mus musculus 56-71 29967158-4 2018 Therefore, we explored the interaction between leptin and endocannabinoid signaling with a focus on fatty acid amide hydrolase (FAAH), the primary degradative enzyme for the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA). aea 190-216 fatty acid amide hydrolase Mus musculus 111-126 29967158-4 2018 Therefore, we explored the interaction between leptin and endocannabinoid signaling with a focus on fatty acid amide hydrolase (FAAH), the primary degradative enzyme for the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA). aea 190-216 fatty acid amide hydrolase Mus musculus 128-132 28910408-8 2017 AEA uptake in both DU145 and RAW264.7 cells was inhibited by FAAH inhibition, but not by COX-2 inhibition, even in RAW264.7 cells where the expression of this enzyme had greatly been induced by lipopolysaccharide + interferon gamma treatment. aea 0-3 fatty acid amide hydrolase Mus musculus 61-65 28234213-3 2017 Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear. aea 73-99 fatty acid amide hydrolase Mus musculus 18-44 28234213-3 2017 Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear. aea 73-99 fatty acid amide hydrolase Mus musculus 46-50 28234213-3 2017 Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear. aea 101-104 fatty acid amide hydrolase Mus musculus 18-44 28234213-3 2017 Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear. aea 101-104 fatty acid amide hydrolase Mus musculus 46-50 28234213-10 2017 CONCLUSION: We propose that the rapid anti-anxiety effects of FAAH inhibition are due to AEA activation of astroglial CB1R and subsequent basolateral amygdala LTD in vivo. aea 89-92 fatty acid amide hydrolase Mus musculus 62-66 28193523-1 2017 Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear. aea 132-158 fatty acid amide hydrolase Mus musculus 73-77 28193523-1 2017 Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear. aea 160-163 fatty acid amide hydrolase Mus musculus 56-71 28193523-1 2017 Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear. aea 160-163 fatty acid amide hydrolase Mus musculus 73-77 25998048-1 2015 Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects. aea 178-181 fatty acid amide hydrolase Mus musculus 14-40 26567045-11 2015 FAAH inhibition increased the efficacy of AEA in primary synoviocytes but not in SFs. aea 42-45 fatty acid amide hydrolase Mus musculus 0-4 25998048-1 2015 Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects. aea 150-176 fatty acid amide hydrolase Mus musculus 14-40 25998048-1 2015 Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects. aea 150-176 fatty acid amide hydrolase Mus musculus 42-46 27385208-9 2016 JZL184 also partially substituted in AEA-trained FAAH mice in the water maze, suggesting incomplete overlap in the stimulus effects of AEA and JZL184. aea 37-40 fatty acid amide hydrolase Mus musculus 49-53 27307500-1 2016 Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects. aea 138-165 fatty acid amide hydrolase Mus musculus 37-52 27307500-1 2016 Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects. aea 138-165 fatty acid amide hydrolase Mus musculus 54-58 27307500-1 2016 Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects. aea 167-171 fatty acid amide hydrolase Mus musculus 37-52 27307500-1 2016 Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects. aea 167-171 fatty acid amide hydrolase Mus musculus 54-58 27109320-1 2016 BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively. aea 147-174 fatty acid amide hydrolase Mus musculus 47-62 27109320-1 2016 BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively. aea 147-174 fatty acid amide hydrolase Mus musculus 64-68 27109320-1 2016 BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively. aea 176-179 fatty acid amide hydrolase Mus musculus 47-62 27109320-1 2016 BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively. aea 176-179 fatty acid amide hydrolase Mus musculus 64-68 27001846-2 2016 We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders. aea 179-182 fatty acid amide hydrolase Mus musculus 114-129 27001846-2 2016 We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders. aea 179-182 fatty acid amide hydrolase Mus musculus 131-135 27001846-4 2016 Using a knock-in mouse model of the FAAH polymorphism that controls for genetic and environmental backgrounds, we confirm phenotypic differences in frontoamygdala circuitry and anxiety-related behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not before. aea 234-237 fatty acid amide hydrolase Mus musculus 36-40 26821211-10 2016 Consistent with these data indicating sustained increases in CRH signaling can mediate the effects of chronic elevations in corticosteroids, CRH overexpressing mice also exhibited increased FAAH-mediated AEA hydrolysis in the amygdala and prefrontal cortex compared to wild type. aea 204-207 fatty acid amide hydrolase Mus musculus 190-194 25998048-1 2015 Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects. aea 178-181 fatty acid amide hydrolase Mus musculus 42-46 22514334-2 2012 Brain enzymatic activity of FAAH and the endogenous levels of its substrates, anandamide (AEA; N-arachidonoylethanolamine), 2-arachidonoylglycerol (2-AG), and N-palmitoylethanolamine (PEA), were measured in control and ST4070-treated mice. aea 95-121 fatty acid amide hydrolase Mus musculus 28-32 25374388-2 2015 Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues. aea 78-81 fatty acid amide hydrolase Mus musculus 11-26 25374388-2 2015 Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues. aea 78-81 fatty acid amide hydrolase Mus musculus 28-32 25374388-2 2015 Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues. aea 114-117 fatty acid amide hydrolase Mus musculus 11-26 25374388-2 2015 Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues. aea 114-117 fatty acid amide hydrolase Mus musculus 28-32 25374388-2 2015 Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues. aea 114-117 fatty acid amide hydrolase Mus musculus 99-103 25058512-2 2014 However, recent preclinical data indicate that combined inhibition of cyclooxygenase (COX) and fatty acid amide hydrolase (FAAH), the primary catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA), produces enhanced antinociceptive effects in a variety of murine models of pain. aea 182-208 fatty acid amide hydrolase Mus musculus 106-121 25058512-2 2014 However, recent preclinical data indicate that combined inhibition of cyclooxygenase (COX) and fatty acid amide hydrolase (FAAH), the primary catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA), produces enhanced antinociceptive effects in a variety of murine models of pain. aea 182-208 fatty acid amide hydrolase Mus musculus 123-127 24849924-1 2014 Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes. aea 241-267 fatty acid amide hydrolase Mus musculus 110-125 24849924-1 2014 Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes. aea 241-267 fatty acid amide hydrolase Mus musculus 127-131 24148808-1 2014 The two most studied endocannabinoids are anandamide (AEA), principally catalyzed by fatty-acid amide hydrolase (FAAH), and 2-arachidonoyl glycerol (2-AG), mainly hydrolyzed by monoacylglycerol lipase (MGL). aea 54-57 fatty acid amide hydrolase Mus musculus 85-111 24148808-1 2014 The two most studied endocannabinoids are anandamide (AEA), principally catalyzed by fatty-acid amide hydrolase (FAAH), and 2-arachidonoyl glycerol (2-AG), mainly hydrolyzed by monoacylglycerol lipase (MGL). aea 54-57 fatty acid amide hydrolase Mus musculus 113-117 22860206-1 2012 Fatty acid amide hydrolase (FAAH) plays the central role in the degradation of bioactive N-acylethanolamines such as the endocannabinoid arachidonoylethanolamide (anandamide) in brain and peripheral tissues. aea 163-173 fatty acid amide hydrolase Mus musculus 11-26 22860205-2 2012 N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). aea 0-26 fatty acid amide hydrolase Mus musculus 179-194 22860205-2 2012 N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). aea 0-26 fatty acid amide hydrolase Mus musculus 196-200 22860206-1 2012 Fatty acid amide hydrolase (FAAH) plays the central role in the degradation of bioactive N-acylethanolamines such as the endocannabinoid arachidonoylethanolamide (anandamide) in brain and peripheral tissues. aea 163-173 fatty acid amide hydrolase Mus musculus 28-32 21719468-3 2011 The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 29-55 fatty acid amide hydrolase Mus musculus 186-201 22927908-6 2012 The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE. aea 138-164 fatty acid amide hydrolase Mus musculus 183-198 22927908-6 2012 The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE. aea 138-164 fatty acid amide hydrolase Mus musculus 200-204 22927908-6 2012 The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE. aea 166-169 fatty acid amide hydrolase Mus musculus 183-198 22927908-6 2012 The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE. aea 166-169 fatty acid amide hydrolase Mus musculus 200-204 21719468-3 2011 The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 29-55 fatty acid amide hydrolase Mus musculus 203-207 20702753-7 2010 Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray. aea 9-12 fatty acid amide hydrolase Mus musculus 51-66 21740924-1 2011 Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors. aea 103-129 fatty acid amide hydrolase Mus musculus 11-26 21740924-1 2011 Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors. aea 103-129 fatty acid amide hydrolase Mus musculus 28-32 20702753-7 2010 Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray. aea 9-12 fatty acid amide hydrolase Mus musculus 68-72 20702753-8 2010 These data indicate that COX-2 possesses the capacity to metabolize AEA in vivo and can compete with FAAH for AEA in several brain regions. aea 110-113 fatty acid amide hydrolase Mus musculus 101-105 20357755-2 2010 However, the consequences of repeated administration of the endocannabinoid N-arachidonoyl ethanolamine (anandamide, AEA) on cannabinoid receptor regulation are unclear because of its rapid metabolism by fatty acid amide hydrolase (FAAH). aea 76-103 fatty acid amide hydrolase Mus musculus 215-230 20375198-2 2010 Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and other conditions. aea 112-138 fatty acid amide hydrolase Mus musculus 23-38 20375198-2 2010 Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and other conditions. aea 112-138 fatty acid amide hydrolase Mus musculus 40-44 20029375-1 2010 RATIONALE: Fatty acid amide hydrolase (FAAH) is the main degrading enzyme of the fatty acid ethanolamides anandamide (AEA) and oleoylethanolamide (OEA), which have opposite effects on food intake and energy balance. aea 118-121 fatty acid amide hydrolase Mus musculus 11-37 20029375-1 2010 RATIONALE: Fatty acid amide hydrolase (FAAH) is the main degrading enzyme of the fatty acid ethanolamides anandamide (AEA) and oleoylethanolamide (OEA), which have opposite effects on food intake and energy balance. aea 118-121 fatty acid amide hydrolase Mus musculus 39-43 20029375-9 2010 As expected, both AEA and OEA levels were increased in hypothalamus, small intestine and liver of FAAH(-/-) mice. aea 18-21 fatty acid amide hydrolase Mus musculus 98-102 20029375-10 2010 CONCLUSION: These results indicate that the lack of FAAH predominantly promotes energy storage by food intake-independent mechanisms, through the enhancement of AEA levels rather than promoting the anorexic effects of OEA. aea 161-164 fatty acid amide hydrolase Mus musculus 52-56 34299330-2 2021 Since the inhibition of fatty acid amide hydrolase (FAAH), the main catabolic enzyme of anandamide (AEA), may provide beneficial effects in mice model of Alzheimer"s disease (AD)-like pathology, we aimed at determining whether the FAAH inhibitor URB597 might target microglia polarization and alter the cytoskeleton reorganization induced by the amyloid-beta peptide (Abeta). aea 100-103 fatty acid amide hydrolase Mus musculus 24-50 19666749-2 2009 N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 0-26 fatty acid amide hydrolase Mus musculus 111-126 19666749-2 2009 N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 0-26 fatty acid amide hydrolase Mus musculus 128-132 19666749-2 2009 N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 28-31 fatty acid amide hydrolase Mus musculus 111-126 19666749-2 2009 N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively. aea 28-31 fatty acid amide hydrolase Mus musculus 128-132 17675189-2 2008 On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects. aea 168-195 fatty acid amide hydrolase Mus musculus 50-65 17675189-2 2008 On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects. aea 168-195 fatty acid amide hydrolase Mus musculus 67-71 16448676-2 2006 Mice lacking the enzyme fatty acid amidohydrolase (FAAH) are severely impaired in their ability to degrade anandamide (AEA) and therefore represent a unique animal model in which to examine the function of AEA in vivo on ethanol-drinking behavior. aea 119-122 fatty acid amide hydrolase Mus musculus 51-55 16448676-2 2006 Mice lacking the enzyme fatty acid amidohydrolase (FAAH) are severely impaired in their ability to degrade anandamide (AEA) and therefore represent a unique animal model in which to examine the function of AEA in vivo on ethanol-drinking behavior. aea 206-209 fatty acid amide hydrolase Mus musculus 51-55 16448676-8 2006 Supersensitivity to exogenous AEA was noted in both male and female FAAH(-/-) mice. aea 30-33 fatty acid amide hydrolase Mus musculus 68-72 15576840-2 2005 Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice. aea 58-61 fatty acid amide hydrolase Mus musculus 8-34 15576840-2 2005 Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice. aea 58-61 fatty acid amide hydrolase Mus musculus 36-40 15576840-2 2005 Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice. aea 157-160 fatty acid amide hydrolase Mus musculus 8-34 15576840-2 2005 Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice. aea 157-160 fatty acid amide hydrolase Mus musculus 36-40 15576840-3 2005 As expected, AEA content in immediately frozen brain tissue was significantly greater in FAAH-deficient (FAAH-/-) than in wild-type mice. aea 13-16 fatty acid amide hydrolase Mus musculus 89-93 15576840-4 2005 However, AEA content was significantly lower in brains from FAAH-/- mice at 5 and 24 h postmortem. aea 9-12 fatty acid amide hydrolase Mus musculus 60-64 15576840-5 2005 Similarly, wild-type mice treated in vivo with a FAAH inhibitor (URB532) had significantly lower brain AEA content 24 h postmortem compared with controls. aea 103-106 fatty acid amide hydrolase Mus musculus 49-53 15576840-6 2005 These data indicate that FAAH contributes significantly to the postmortal accumulation of AEA. aea 90-93 fatty acid amide hydrolase Mus musculus 25-29 15576840-9 2005 These data demonstrate that FAAH activity differentially affects AEA and OEA/PEA contents postmortem and suggest that AEA formation specifically occurs via an ethanolamine-dependent route postmortem. aea 65-68 fatty acid amide hydrolase Mus musculus 28-32 15576840-9 2005 These data demonstrate that FAAH activity differentially affects AEA and OEA/PEA contents postmortem and suggest that AEA formation specifically occurs via an ethanolamine-dependent route postmortem. aea 118-121 fatty acid amide hydrolase Mus musculus 28-32 34916909-2 2021 One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH). aea 28-54 fatty acid amide hydrolase Mus musculus 109-124 34916909-2 2021 One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH). aea 28-54 fatty acid amide hydrolase Mus musculus 126-130 34916909-2 2021 One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH). aea 68-71 fatty acid amide hydrolase Mus musculus 109-124 34916909-2 2021 One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH). aea 68-71 fatty acid amide hydrolase Mus musculus 126-130 34587978-5 2021 In the 5xFAD model, the genetic inactivation of the enzyme that degrades anandamide (AEA), the fatty acid amide hydrolase (FAAH), was associated with a significant amelioration of the memory deficit. aea 85-88 fatty acid amide hydrolase Mus musculus 123-127 19647115-4 2009 Recently, we have shown that treatment of mouse primary Sertoli cells with FSH enhances the activity of the AEA hydrolase (fatty acid amide hydrolase, FAAH), whereas it does not affect the enzymes that synthesize AEA, nor the level of the AEA-binding type-2 cannabinoid and type-1 vanilloid receptors. aea 108-111 fatty acid amide hydrolase Mus musculus 151-155 17110429-8 2007 Finally, we demonstrate that FSH protects Sertoli cells against the pro-apoptotic activity of AEA, through PKA and aromatase-dependent activation of FAAH. aea 94-97 fatty acid amide hydrolase Mus musculus 149-153 15157693-1 2004 Although the N-arachidonoyl ethanolamine (anandamide) binds to cannabinoid receptors and has been implicated in the suppression of pain, its rapid catabolism in vivo by fatty acid amide hydrolase (FAAH) has presented a challenge in investigating the physiological functions of this endogenous cannabinoid. aea 13-40 fatty acid amide hydrolase Mus musculus 197-201 34587978-5 2021 In the 5xFAD model, the genetic inactivation of the enzyme that degrades anandamide (AEA), the fatty acid amide hydrolase (FAAH), was associated with a significant amelioration of the memory deficit. aea 85-88 fatty acid amide hydrolase Mus musculus 95-121 34299330-2 2021 Since the inhibition of fatty acid amide hydrolase (FAAH), the main catabolic enzyme of anandamide (AEA), may provide beneficial effects in mice model of Alzheimer"s disease (AD)-like pathology, we aimed at determining whether the FAAH inhibitor URB597 might target microglia polarization and alter the cytoskeleton reorganization induced by the amyloid-beta peptide (Abeta). aea 100-103 fatty acid amide hydrolase Mus musculus 52-56 32416152-2 2020 Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively. aea 157-160 fatty acid amide hydrolase Mus musculus 0-26 32416152-2 2020 Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively. aea 157-160 fatty acid amide hydrolase Mus musculus 28-32 30421483-4 2019 In both genotypes, EtOH treatment caused no changes in baseline endocannabinoid levels, although FAAH KO mice displayed higher baseline N-arachidonoylethanolamine levels than WT mice. aea 136-162 fatty acid amide hydrolase Mus musculus 97-101 30532004-6 2019 This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged. aea 189-192 fatty acid amide hydrolase Mus musculus 30-34 28104279-2 2019 The endocannabinoid system is known to modulate the nigrostriatal pathway through endogenous ligands such as anandamide (AEA), which is hydrolysed by fatty acid amide hydrolase (FAAH). aea 121-124 fatty acid amide hydrolase Mus musculus 161-176 28104279-2 2019 The endocannabinoid system is known to modulate the nigrostriatal pathway through endogenous ligands such as anandamide (AEA), which is hydrolysed by fatty acid amide hydrolase (FAAH). aea 121-124 fatty acid amide hydrolase Mus musculus 178-182 35316021-4 2022 While MAGL inhibitors upregulate 2-acyl glycerol (2-AG) levels and reduce neuroinflammation, FAAH inhibitors elevate anandamide (AEA) levels and prevent the degradation of HSP-70, thereby preventing the phosphorylation of tau protein and formation of NFTs in neural cells. aea 129-132 fatty acid amide hydrolase Mus musculus 93-97 33833828-3 2021 Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH). aea 42-45 fatty acid amide hydrolase Mus musculus 143-158 33833828-3 2021 Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH). aea 42-45 fatty acid amide hydrolase Mus musculus 160-164 33490317-2 2021 In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice. aea 198-201 fatty acid amide hydrolase Mus musculus 125-151 33490317-2 2021 In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice. aea 198-201 fatty acid amide hydrolase Mus musculus 153-157 32860981-1 2020 Fatty acid amide hydrolase (FAAH) exerts its main function in the catabolism of the endogenous chemical messenger anandamide (AEA), thus modulating the endocannabinoid (eCB) pathway. aea 126-129 fatty acid amide hydrolase Mus musculus 0-26 32860981-1 2020 Fatty acid amide hydrolase (FAAH) exerts its main function in the catabolism of the endogenous chemical messenger anandamide (AEA), thus modulating the endocannabinoid (eCB) pathway. aea 126-129 fatty acid amide hydrolase Mus musculus 28-32 32860981-5 2020 Herein, we have identified a new FAAH inhibitor (1-((1-methyl-1H-indol-2-yl)methyl)piperidin-4-yl)(oxazol-2-yl)methanone (8) which inhibits the hydrolysis of AEA in the brain with high potency (IC50 value 11 nM at a substrate concentration of 0.5 microM), and without showing time-dependency. aea 158-161 fatty acid amide hydrolase Mus musculus 33-37