ライフサイエンスコーパス: AEA

1 AEA acts as an endocannabinoid and an endovanilloid by a

2 AEA analysis was linear over the range 0.23 to 19 nM (1.

3 AEA caused a significant decrease in cell number only at

4 AEA did not significantly alter 5-HT(3A) receptor traffi

5 AEA has been isolated from numerous tissues and biofluid

6 AEA hydrolysis was detectable at the earliest measurable

7 AEA is hydrolyzed by fatty acid amide hydrolase (FAAH),

8 AEA significantly inhibited cytokine production from hea

9 AEA uptake and hydrolysis were significantly potentiated

10 AEA was analyzed in cord and maternal blood, amniotic fl

11 AEA was detected in serum and plasma from blood isolated

12 AEA was found to induce a preferential processing of Not

13 AEA was readily trafficked to lipid droplets, confirming

14 AEA was undetectable in saliva and urine.

15 AEA-treated keratinocytes showed reduced an induction of

16 2 knockdown in dCAD cells did not affect [3H]AEA uptake.

17 increase in the overall levels of intact [3H]AEA associated with the cells, suggesting that trafficki

18 he cells, suggesting that trafficking of [3H]AEA to FAAH had been disrupted.

19 Results using the [(2)H(4)]AEA and HPLC-MS/MS method agreed well with those obtaine

20 eukocyte assay using stably labeled [(2)H(4)]AEA as substrate.

21 The 60% AEA extraction efficiency achieved with SPE from plasma

22 ous studies have mapped anti-erythrocyte Ab (AEA)-promoting NZB loci to several chromosomal locations

23 validated method using octa-deuterated AEA (AEA-d8) as an internal standard represents an improvemen

24 differentially modulates brain lipid (2-AG, AEA, and OEA) signaling, and these modulations are influ

25 2-AG, AEA, and WIN55,212-2, enhanced Galpha(i/o) and Gbetagamm

26 2-AG, AEA, THC, and WIN55,212-2 also activated Galpha(q)-depen

27 e alpha2 subunit converted the alpha1/alpha3 AEA-sensitive receptors to sensitivity resembling that o

28 Although AEA and 2-AG likely subserve distinct physiological role

29 k suggests that rapid reductions in amygdala AEA signaling following stress may prime the amygdala an

30 s the existence and the activity of FAAH, an AEA-metabolizing enzyme, in the TM tissues.

31 , we develop Annotation Enrichment Analysis (AEA), which properly accounts for the non-uniformity of

32 Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most char

33 Anandamide (AEA) and other bioactive N-acylethanolamines (NAEs) are

34 Anandamide (AEA) is an endogenous intestinal cannabinoid that contro

35 Anandamide (AEA) is an endogenous ligand of cannabinoid receptors an

36 h 2-arachidonoylglycerol (2-AG), anandamide (AEA), CP55,940, Delta(9)-tetrahydrocannabinol (THC), can

37 ndogenous CB1 receptor agonists, anandamide (AEA), increases during development in whole-brain sample

38 -arachidonoylglycerol (2-AG) and anandamide (AEA) activate a canonical cannabinoid receptor in Caenor

39 -arachidonyl glycerol (2-AG) and anandamide (AEA)), two synthetic cannabinoids (WIN55,212-2 and CP55,

40 iny neurons (MSNs) with the eCBs anandamide (AEA) or 2-arachidonoylglycerol and determined the condit

41 We show that the endocannabinoid anandamide (AEA) can alter neuronal cell function both through its e

42 we show that the endocannabinoid anandamide (AEA) is a key mediator of hypoxic pulmonary vasoconstric

43 H), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbi

44 ar uptake of the endocannabinoid anandamide (AEA) occurs has been the source of much debate.

45 ubation with the endocannabinoid anandamide (AEA) substantially increased the amplitude of glycine-ac

46 he levels of the endocannabinoid anandamide (AEA) when administered to humans, suggesting that phytoc

47 s, including the endocannabinoid anandamide (AEA), is principally mediated by the integral membrane e

48 reduction in the endocannabinoid anandamide (AEA), within the amygdala.

49 sporters for the endocannabinoid anandamide (AEA).

50 trations of the endocannabinoid, anandamide (AEA), in both their plasma and their endometrial tissue

51 ect of the main endocannabinoid, anandamide (AEA), in these DC subsets and correlated cytokine levels

52 ned whether the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are released by

53 e the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG), respectively, ha

54 f levels of the endocannabinoids anandamide (AEA) or 2-arachidonoylglycerol (2-AG) in the rACC follow

55 cells secrete endocannabinoids, anandamide (AEA) (35 pg/10(7) cells), and 2-AG (75.2 ng/10(7) cells)

56 The two endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), play independent

57 fluence of the endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol, on the Notch-1 pathway

58 ermine the effects of endogenous anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) on the permeabil

59 s signaling lipids that includes anandamide (AEA).

60 mal melanocyte cells), including anandamide (AEA), 2-arachidonoylglycerol, the respective target rece

61 ces neurodegeneration, increased anandamide (AEA) but not 2-arachidonylglycerol biosynthesis and CB1R

62 ne-naive controls, and increased anandamide (AEA) release during nicotine intake.

63 CB2), their endogenous ligands, anandamide (AEA) and 2-arachidonoylglycerol, and metabolic enzymes o

64 hanges in the two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), with stress exp

65 e research on the trafficking of anandamide (AEA) across cell membranes, little is known about the me

66 the anti-hyperalgesic effects of anandamide (AEA) and cyclohexylcarbamic acid 3'-carbamoyl-biphenyl-3

67 with a decrease in the level of anandamide (AEA) in plantar paw skin ipsilateral to tumors.

68 was accompanied by a decrease of anandamide (AEA) levels in the amygdala and prefrontal cortex, and t

69 lular CB1R-dependent signalling, anandamide (AEA) has come to the forefront in several novel contexts

70 ging evidence has suggested that anandamide (AEA), an endogenous agonist of cannabinoid (CB) receptor

71 JZL184 (0.1-1 mug/side), and the anandamide (AEA) hydrolysis inhibitor URB597 (10-30 ng/side) were ad

72 plored this possibility by using anandamide (AEA), an endogenously produced cannabinoid that has been

73 2-arachidonylglycerol [2-AG] and anandamide [AEA]) in 3T3-L1 adipocytes.

74 aling, we measured the amount of anandamide [AEA (N-arachidonoylethanolamine)] and 2-arachidonoylglyc

75 modulated by the endocannabinoid anandamide(AEA) and its receptors: cannabinoid-1 (CB1), cannabinoid

76 2-AG and AEA displayed Galphai/o/Gbetagamma bias and normalized C

77 i/o) and Gbetagamma signaling, with 2-AG and AEA treatment leading to increased total CB1 levels.

78 increased plasma EC concentrations (2-AG and AEA) and elevated adipose tissue 2-AG.

79 f acute stress to modulate amygdala FAAH and AEA in both rats and mice is also mediated through CRHR1

80 jor psychoactive component of marijuana, and AEA.

81 anandamide [i.e., arachidonoylethanolamide (AEA)] has been attributed to reduced activity of the AEA

82 sts CP55,940 and N-arachidonoylethanolamine (AEA).

83 N-Arachidonoylethanolamine (AEA, anandamide) was the first endocannabinoid to be ide

84 Anandamide (N-arachidonoylethanolamine, AEA) is an endocannabinoid present in human plasma that

85 noid anandamide (N-arachidonoylethanolamine, AEA).

86 abinoid anandamide (arachidonylethanolamide, AEA) on the function of alpha4beta2 nicotinic acetylchol

87 ration of the eCB N-arachidonylethanolamine (AEA) within the amygdala.

88 d via anandamide (N-arachidonylethanolamine [AEA]) and 2-arachidonoylglycerol (2-AG) in the regulatio

89 ecule capsaicin (CP) has a similar effect as AEA; however, CP acts by engagement of the vanilloid rec

90 Consistent with the roles of FABP as AEA carriers, administration of the competitive FABP lig

91 on-lipid FABP inhibitor BMS309403 attenuated AEA uptake and hydrolysis by approximately 50% in N18TG2

92 Because AEA and 2-AG undergo rapid and almost complete intracell

93 unique among neuro/immune modulators because AEA, an uncharged hydrophobic molecule, diffuses into ce

94 otentially wider therapeutic overlap between AEA and 2-AG augmentation approaches than was previously

95 nxiety and the functional redundancy between AEA and 2-AG signaling in the modulation of anxiety-like

96 Both CB(1) (by AEA and 2-AG) and non-CB(1) (by OEA) targets can alter t

97 atinocytes, and found that CB1 activation by AEA suppressed production and release of signature TH1-

98 ly emphasized when ECS was hyperactivated by AEA and in ob/ob tissue.

99 ibited the potentiation of I(Gly) induced by AEA and THC.

100 onsiveness to cytokine inhibition induced by AEA.

101 n the enhanced Notch-1 signaling mediated by AEA.

102 Notch-1, numb (Nb), this can be prevented by AEA and 2-arachidonoylglycerol.

103 The inhibition of 5-HT(3) receptors by AEA may contribute to its physiological roles in control

104 other three rate constants were unaltered by AEA suggested that AEA raised the energy of the activate

105 , arachidonoyl-[1-(14)C]ethanolamide ([(14)C]AEA) uptake, and FABP knockdown to demonstrate that tran

106 (5 mum), a functional synergism on cellular AEA and 2-AG uptake was observed.

107 l membrane transporter controls the cellular AEA and 2-AG trafficking and metabolism.

108 unt for the observed increase in circulating AEA in humans following CBD consumption.

109 We also show that at higher concentrations AEA induces normal human epidermal melanocyte apoptosis

110 However, at lower concentrations, AEA and other CB(1)-binding endocannabinoids dose-depend

111 s efficacious in potentiating I(Gly), desoxy-AEA inhibited potentiation produced by both Delta(9)-tet

112 While desoxy-AEA was significantly less efficacious in potentiating I

113 fully validated method using octa-deuterated AEA (AEA-d8) as an internal standard represents an impro

114 to the anti-hyperalgesic effect of elevated AEA levels.

115 alpha4beta2 nAChR function by an endogenous AEA-like lipid.

116 e results of this study show that endogenous AEA and 2-AG production and CB1 activation play a key mo

117 940 to the CB1 receptor as well as enhancing AEA-stimulated [(35)S]GTPgammaS binding in mouse brain m

118 endocannabinoids, arachidonyl ethanolamide (AEA) and 2-arachidonylglycerol (2-AG), to prostaglandin-

119 inoid anandamide (arachidonoyl ethanolamide, AEA) is an uncharged neuromodulatory lipid that, similar

120 Our aims were to (1) evaluate AEA levels at the human maternal:fetal interface and (2)

121 However, to pharmacologically exploit AEA and/or 2-AG signaling in this way, we must first gai

122 Limits of quantification and detection for AEA were also improved dramatically using SPE (8 and 4 f

123 fficient cytosolic trafficking mechanism for AEA.

124 tal issues such as the synthesis pathway for AEA and the molecular mechanism(s) underlying cellular u

125 ences in nine discrete rat brain regions for AEA, 2-AG, 2-LG, OEA, PEA, noladin ether, virodhamine, a

126 Here, we uncover a role for AEA and its receptor, cannabinoid receptor 2 (CB2), in t

127 ggesting that FAAH protects hepatocytes from AEA-induced cell death in vivo.

128 wever, these animals eventually recover from AEA treatment, implying the existence of alternative rou

129 for tissues spiked with 0.2, 1, and 5pmol/g AEA of less than 12%.

130 y for fatty acid ethanolamide ligands (e.g., AEA) evolved thereafter.

131 eed well with those obtained using the [(3)H]AEA radiometric assay.

132 at leukocyte FAAH activity assay using [(3)H]AEA, we have developed a human leukocyte assay using sta

133 Postmenopausal women had AEA concentrations comparable to levels observed during

134 ediating the HFD-induced increase in hepatic AEA, which then activates hepatic CB1R to induce insulin

135 e we show that HFD-induced increased hepatic AEA levels and decreased FAAH activity are absent in SCD

136 of hepatic FAAH activity, normalizes hepatic AEA levels, and improves insulin sensitivity.

137 nt cancer cell lines die in response to high AEA concentrations.

138 Higher AEA concentrations were found in placenta compared to fe

139 However, AEA accelerated 5-HT(3A) receptor desensitization time i

140 omogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities appr

141 In contrast, FAAH-2 hydrolyzed AEA and PEA in intact cells with rates approximately 30-

142 onist, arachidonic acid N-hydroxyethylamide (AEA), indicating the effectiveness of treatments in modu

143 ivity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their n

144 The relevance of these changes in AEA concentrations at the maternal:fetal interface requi

145 re sufficient to evoke phenotypic changes in AEA signaling in DRG neurons.

146 tudies have demonstrated that the decline in AEA appears to contribute to the manifestation of the st

147 The decrease in AEA occurred in conjunction with increased degradation o

148 ies indicate that FAAH-mediated decreases in AEA occur following chronic stress and that this loss of

149 enzyme fatty acid amide hydrolase (FAAH) in AEA-induced cell death in the liver.

150 rmine whether this developmental increase in AEA also takes place in striatal tissue and whether incr

151 ty blocked the training-induced increases in AEA levels as well as the memory enhancement produced by

152 strated the involvement of these proteins in AEA-induced melanogenesis.

153 Significant variability in AEA plasma concentrations has been reported between stud

154 congenic mice exhibited marked reductions in AEAs and splenomegaly but not in anti-nuclear Abs.

155 res with the FAAH inhibitor URB597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive mann

156 ace in striatal tissue and whether increased AEA levels contribute to the postnatal switch in the res

157 Inhibition of FAAH activity increases AEA concentrations in nervous tissue and reduces sensory

158 nhibitor URB597, which selectively increases AEA levels at active synapses, administered into the bas

159 that emotionally arousing training increases AEA levels within prefrontal-limbic circuits and strongl

160 s the source responsible for hypoxia-induced AEA generation.

161 Interestingly, AEA up-regulated Nct expression, a component of gamma-se

162 rain were examined as possible intracellular AEA carriers.

163 increases in anxiety associated with limbic AEA deficiency.

164 Mean AEA concentrations were 2.72 + or - 1.04 pmol/g for plac

165 ay variability were comparable, and the mean AEA concentration of pooled plasma samples (1.18 nM, n=1

166 BPs) are intracellular proteins that mediate AEA transport to its catabolic enzyme fatty acid amide h

167 in almost 70% death after 24 h at 50 microm AEA and lowering the threshold for cell death to 500 nm.

168 e concentration range of 200 nM to 2 microM, AEA significantly reduced the maximal amplitudes and inc

169 Multiple AEA-induced metabolites were observed in brains from FAA

170 B597, an FAAH inhibitor, the effect of 10 nM AEA on outflow facility was prolonged by at least 4 hour

171 In human U937 leukemia cells, 100 nm AEA and 1 mum 2-AG were taken up through a fast and satu

172 yed an increase in hippocampal 2-AG, but not AEA, levels at the time of retention testing and a decre

173 Accumulation of AEA and 2-AG was achieved by inhibiting their metabolizi

174 P5 in mice results in excess accumulation of AEA, abolishes PPARbeta/delta activation in the brain, a

175 The actions of AEA were apparent when applied extracellularly but not d

176 activity studies, the enzymatic activity of AEA hydrolysis was detected in TM tissues, and this acti

177 t to rimonabant,the I.C.V. administration of AEA (50 mug) enhanced LPS hypothermia.

178 Administration of AEA caused a transient enhancement of aqueous humor outf

179 study demonstrate that the administration of AEA increases aqueous humor outflow facility and that th

180 rons) to determine whether administration of AEA results in abnormal responses of group IV afferent n

181 Further, oral administration of AEA to NOD mice provides protection from T1D.

182 of biomatrices containing limited amounts of AEA.

183 Further analysis of AEA effects on alpha4beta2 nAChR-mediated currents, usin

184 this method is suitable for the analysis of AEA in clinical samples and may be utilised for the inve

185 method is described here for the analysis of AEA in human plasma.

186 by selective pharmacological augmentation of AEA signaling and via direct cannabinoid receptor 1 stim

187 nhibit the cellular uptake and catabolism of AEA by targeting FABPs.

188 in conjunction with increased degradation of AEA by fatty acid amide hydrolase (FAAH).

189 sional barrier for the efficient delivery of AEA to its site of catabolism.

190 conclusion, FAAH and GSH are determinants of AEA-mediated cell death in the liver.

191 sclose a distinct immunomodulatory effect of AEA in mDCs and pDCs from MS patients, which may reflect

192 mor outflow facility and that this effect of AEA involves CB1 and CB2 cannabinoid receptors.

193 by the prominent vasoconstrictive effect of AEA on pulmonary arteries and strongly reduced HPV in FA

194 The effect of AEA was measured at different timepoints (4, 18, 24, 48,

195 Furthermore, the effects of AEA ACh currents were not altered by the calcium chelato

196 oreactivity as well as inhibitory effects of AEA and URB597 on the depolarization-evoked Ca(2+) trans

197 mportantly, the anti-hyperalgesic effects of AEA and URB597 were blocked by a CB1 receptor antagonist

198 The effects of AEA could be neither replicated by the exogenous cannabi

199 The effects of AEA on aqueous humor outflow were measured using a porci

200 The stimulatory effects of AEA on Notch-1 signaling persisted in the presence of Ab

201 We aimed to investigate the effects of AEA on the survival and proliferation of an endometrial

202 sensitized to the pharmacological effects of AEA; however, these animals eventually recover from AEA

203 a robust SPE technique for the extraction of AEA from biomatrices to replace the existing liquid extr

204 alidate the use of solid-phase extraction of AEA from tissues.

205 suggest that pharmacological facilitation of AEA signaling is a promising strategy for attenuating ci

206 FABP5 both promotes the hydrolysis of AEA into arachidonic acid and thus reduces brain endocan

207 ry measurements revealed a clear increase of AEA and the FAAH-dependent metabolite arachidonic acid i

208 sked at 5 min with appreciable inhibition of AEA accumulation correlating with partial inhibition of

209 ation correlating with partial inhibition of AEA hydrolysis.

210 iphenyl-3-yl ester (URB597), an inhibitor of AEA hydrolysis.

211 Intraplantar injection of AEA (10 mug/10 mul) or URB597 (9 mug/10 mul) transiently

212 lar responses to intra-arterial injection of AEA into the hindlimb of normal, cardiomyopathic and neo

213 Intraplantar injection of AEA reduced the hyperalgesia, and intraplantar injection

214 action (SPE) method for the investigation of AEA concentrations in human plasma, serum, milk, urine,

215 ibitor of FAAH, increased the local level of AEA and also reduced hyperalgesia.

216 re accompanied by a decrease in the level of AEA in plantar paw skin.

217 lipopolysaccharide (LPS), elevated levels of AEA (75.6 pg/10(7) cells) and 2-AG (98.8 ng/10(7) cells)

218 shock intensity produced increased levels of AEA in the amygdala, hippocampus, and medial prefrontal

219 id 1 receptor density or change in levels of AEA or 2-AG.

220 a pronounced increase in striatal levels of AEA, but not the other major endogenous cannabinoid 2-ar

221 AH)(-/-) mice, which have elevated levels of AEA, yielded increased colony formation as compared with

222 llowing chronic stress and that this loss of AEA signaling is functionally relevant to the effects of

223 urface receptor expression, the magnitude of AEA inhibition decreased.

224 The magnitude of AEA inhibition was inversely correlated with the express

225 tamine (5-HT) and increased the magnitude of AEA inhibition.

226 desensitization and reduced the magnitude of AEA inhibition.

227 The magnitude of AEA potentiation decreased with removal of either the hy

228 Pharmacological manipulation of AEA and 2-AG signaling should prove to have significant

229 ulness of this method for the measurement of AEA levels in clinical samples, plasma samples obtained

230 out the molecular and cellular mechanisms of AEA-induced direct effects on LGICs.

231 OMDM-2 inhibit the bidirectional movement of AEA and 2-AG across cell membranes.

232 desensitization kinetics and the potency of AEA-induced inhibiting effect on the receptors.

233 esults directly demonstrated the presence of AEA-specific promoting genes on NZB chromosome 4, docume

234 receptor TRPV1, causing local production of AEA, which acts through CB2.

235 d between studies, because quantification of AEA is fraught with methodological difficulties.

236 cells were cultured in vitro, and a range of AEA concentrations (0-10 000 nM) were added to the cells

237 ibitors also blocked the cellular release of AEA and 2-AG.

238 The substrate specificity of AEA compared to those of PG-Gs was approximately 200-300

239 nd events responsible for the termination of AEA and 2-AG signaling.

240 on and GSH depletion had additive effects on AEA-mediated hepatocyte cell death resulting in almost 7

241 l of either the hydroxyl or oxygen groups on AEA.

242 mice showed that the full effect of Lbw2 on AEA production was dependent on three subloci, with sple

243 2-AG or AEA activate NPR-19 directly and cannabinoid-dependent i

244 2-AG or AEA inhibit nociception and feeding through a pathway re

245 urified MGL and FAAH compared to 2-AG and/or AEA.

246 as determined to be O-phosphorylcholine (PC)-AEA.

247 Plasma AEA concentrations were significantly (P=0.0078) lower i

248 The highest plasma AEA levels were observed in women in active labour, and

249 To study this process, AEA uptake and hydrolysis were examined in COS-7 cells e

250 n the current study, none of these purported AEA transporter inhibitors affected uptake at 25 s.

251 putative transport inhibitors did not reduce AEA uptake in FAAH chemical knock-out cells.

252 ycerol (2-AG), with stress exposure reducing AEA levels and increasing 2-AG levels.

253 ngly suggests that the endogenously released AEA modulates memory consolidation.

254 he robust developmental increase in striatal AEA may be the key factor in the emergence of HFS-induce

255 In summary, AEA has the proclivity to enhance Notch-1 signaling in a

256 Furthermore, application of synthetic AEA during HFS in field recordings of slices from P12-P1

257 and were significantly (P=0.0389) lower than AEA plasma concentrations obtained during the follicular

258 en together, these findings demonstrate that AEA suppresses highly pathogenic T cell subsets through

259 We determined that AEA controls changes in blood pressure, predominately vi

260 These data indicate that AEA and 2-AG signaling pathways interact to regulate spe

261 These results indicate that AEA directly inhibits the function of alpha4beta2 nAChRs

262 Taken together, these findings indicate that AEA-mediated activation of CB(1) receptors is crucial fo

263 nse to AEA in NNCAP animals, indicating that AEA is acting on group IV afferent neurons in this prepa

264 s not treated with LPS, thus indicating that AEA modulates LPS-activated pathways in the brain rather

265 Here, we report that AEA inhibited the function of serotoningated ion channel

266 We report that AEA up-regulates Notch-1 signaling in cultured neurons.

267 Our results show that AEA induces a decrease in Ishikawa cell number probably

268 We show that AEA is able to identify biologically meaningful function

269 nstants were unaltered by AEA suggested that AEA raised the energy of the activated state.

270 The AEA-induced enhancement of outflow facility was blocked

271 The AEA/CB1R/pERK1/2 signaling pathway may be directly respo

272 bohydrate and lipid metabolism, blunting the AEA-induced increase in gene expression of proteins rela

273 d nearly 30-fold as a linear function of the AEA concentration.

274 The onset and washout of the AEA effects required several minutes (10-30 min), but th

275 ith hydrolase-inactive concentrations of the AEA transport inhibitors UCM707 (1 mum) and OMDM-2 (5 mu

276 this study, we investigated the role of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) i

277 s been attributed to reduced activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH).

278 restored at 48 and 72 h suggesting that the AEA growth inhibitory effect is time limiting.

279 Thus, the AEA/FAAH pathway is an important mediator of HPV and is

280 desensitization time was correlated with the AEA-induced inhibiting effect and mean 5-HT current dens

281 Therefore, AEA likely traverses the cytosol with the assistance of

282 Tissue AEA was quantified using an isotope-dilution method and

283 suggest that the increased plasma and tissue AEA concentrations observed in patients with endometrial

284 alpha2 subunit was relatively insensitive to AEA.

285 els of FAAH and were completely resistant to AEA-induced cell death, whereas primary hepatic stellate

286 bserved a reduced blood pressure response to AEA in NNCAP animals, indicating that AEA is acting on g

287 observed that the blood pressure response to AEA is blunted in cardiomyopathic rats when compared to

288 levels of FAAH and were highly sensitive to AEA-induced cell death.

289 and alpha3 subunits were highly sensitive to AEA-induced potentiation, the alpha2 subunit was relativ

290 Ishikawa cells were sensitive to AEA-mediated cytotoxicity in a pseudo dose-dependent man

291 signaling coordinates a disruption of tonic AEA activity to promote a state of anxiety, which in tur

292 resent the first proteins known to transport AEA from the plasma membrane to FAAH for inactivation an

293 served when uptake was plotted using unbound AEA at 37 degrees C.

294 Intriguingly, structurally unrelated AEA uptake inhibitors also blocked the cellular release

295 on of FAAH can have a pronounced effect upon AEA uptake.

296 e (FAAH) does not appreciably affect uptake, AEA accumulated via a nonsaturable mechanism at 37 degre

297 ted behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not b

298 e, Ishikawa, contains the receptors to which AEA binds.

299 r N-acylethanolamines did not interfere with AEA and 2-AG uptake.

300 he metabolome of FAAH(-/-) mice treated with AEA.