ライフサイエンスコーパス: anandamide

1 onoylglycerol and N-arachidonylethanolamide (anandamide).

2 noyl glycerol and arachidonoyl ethanolamide (anandamide).

3 -nociceptive stimuli were unaffected 2-AG or anandamide.

4 e endocannabinoids 2-arachidonoylglycerol or anandamide.

5 umulation of 2-AG without altering levels of anandamide.

6 inoid (EC), noladin ether (NLDE), but not by anandamide.

7 ability and actions may differ from those of anandamide.

8 firing facilitated uptake and degradation of anandamide.

9 e for the degradation of the endocannabinoid anandamide.

10 nuated the excitation produced by 100 microg anandamide.

11 oxidative metabolism of the endocannabinoid anandamide.

12 naling lipids, including the endocannabinoid anandamide.

13 t also a reduction in cortical and amygdalar anandamide.

14 ary catabolic enzyme for the endocannabinoid anandamide.

15 elay of plasma glucose appearance induced by anandamide.

16 tsynaptic endocannabinoid release, likely of anandamide.

17 ty, functional potency, and efficacy of meth-anandamide, 2-arachidonoyl glycerol, virodhamine, Noladi

18 Peripheral levels of anandamide, 2-arachidonoylglycerol, oleoylethanolamide,

19 Peripheral concentrations of anandamide, 2-arachidonoylglycerol, oleoylethanolamide,

20 URB597 treatment increased levels of anandamide, 2-arachidonyl glycerol, and oleoyl ethanolam

21 We report that the 5,6-epoxide of anandamide, 5,6-epoxyeicosatrienoic acid ethanolamide (5

22 levated levels ofN-arachidonyl ethanolamide (anandamide), a major endocannabinoid lipid mediator, wer

23 In contrast, anandamide, a blocker of connexin gap junction channels,

24 ve pharmacology, we extend these findings to anandamide, a promiscuous endocannabinoid/endovanilloid

25 atment of dCAD cells significantly inhibited anandamide accumulation.

26 the endogenous TRPV1 and CB1 receptor ligand anandamide (ACR neurons).

27 oma x glioma cells, we provide evidence that anandamide acting on CB(1) receptors increases intracell

28 t BM stromal cells secrete endocannabinoids, anandamide (AEA) (35 pg/10(7) cells), and 2-AG (75.2 ng/

29 ite extensive research on the trafficking of anandamide (AEA) across cell membranes, little is known

30 r agonists 2-arachidonoylglycerol (2-AG) and anandamide (AEA) activate a canonical cannabinoid recept

31 first examined whether the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are

32 y was to determine the effects of endogenous anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) on t

33 irectional changes in the two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), wit

34 Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are t

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

36 that regulate the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG), resp

37 d 2 (CB1 and CB2), their endogenous ligands, anandamide (AEA) and 2-arachidonoylglycerol, and metabol

38 study the influence of the endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol, on the Notc

39 nvestigated the anti-hyperalgesic effects of anandamide (AEA) and cyclohexylcarbamic acid 3'-carbamoy

40 Anandamide (AEA) and other bioactive N-acylethanolamines

41 , which induces neurodegeneration, increased anandamide (AEA) but not 2-arachidonylglycerol biosynthe

42 We show that the endocannabinoid anandamide (AEA) can alter neuronal cell function both t

43 for intercellular CB1R-dependent signalling, anandamide (AEA) has come to the forefront in several no

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

45 s associated with a decrease in the level of anandamide (AEA) in plantar paw skin ipsilateral to tumo

46 Herein, we show that the endocannabinoid anandamide (AEA) is a key mediator of hypoxic pulmonary

47 Anandamide (AEA) is an endogenous intestinal cannabinoid

48 Anandamide (AEA) is an endogenous ligand of cannabinoid

49 withdrawal was accompanied by a decrease of anandamide (AEA) levels in the amygdala and prefrontal c

50 drolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of

51 h the cellular uptake of the endocannabinoid anandamide (AEA) occurs has been the source of much deba

52 Analysis of levels of the endocannabinoids anandamide (AEA) or 2-arachidonoylglycerol (2-AG) in the

53 al medium spiny neurons (MSNs) with the eCBs anandamide (AEA) or 2-arachidonoylglycerol and determine

54 ve to nicotine-naive controls, and increased anandamide (AEA) release during nicotine intake.

55 ustained incubation with the endocannabinoid anandamide (AEA) substantially increased the amplitude o

56 HC elevate the levels of the endocannabinoid anandamide (AEA) when administered to humans, suggesting

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

58 human epidermal melanocyte cells), including anandamide (AEA), 2-arachidonoylglycerol, the respective

59 Converging evidence has suggested that anandamide (AEA), an endogenous agonist of cannabinoid (

60 We explored this possibility by using anandamide (AEA), an endogenously produced cannabinoid t

61 reatment with 2-arachidonoylglycerol (2-AG), anandamide (AEA), CP55,940, Delta(9)-tetrahydrocannabino

62 vated concentrations of the endocannabinoid, anandamide (AEA), in both their plasma and their endomet

63 ated the effect of the main endocannabinoid, anandamide (AEA), in these DC subsets and correlated cyt

64 he primary endogenous CB1 receptor agonists, anandamide (AEA), increases during development in whole-

65 ing molecules, including the endocannabinoid anandamide (AEA), is principally mediated by the integra

66 ch causes a reduction in the endocannabinoid anandamide (AEA), within the amygdala.

67 ellular transporters for the endocannabinoid anandamide (AEA).

68 of endogenous signaling lipids that includes anandamide (AEA).

69 abinoid signaling, we measured the amount of anandamide [AEA (N-arachidonoylethanolamine)] and 2-arac

70 llular ECs (2-arachidonylglycerol [2-AG] and anandamide [AEA]) in 3T3-L1 adipocytes.

71 de (LPS) is modulated by the endocannabinoid anandamide(AEA) and its receptors: cannabinoid-1 (CB1),

72 , we determined if intraplantar injection of anandamide altered withdrawal responses to radiant heat.

73 evels of both beta-endorphin (an opioid) and anandamide (an endocannabinoid).

74 Mice were injected intraperitoneally with anandamide, an endocannabinoid binding both CB1R and CB2

75 ver, that changed dramatically in 1993, when anandamide, an NAE of arachidonic acid (N-arachidonyleth

76 on by various cannabinoids (Delta(9)THC, the anandamide analog methanandamide, and JWH015) increases

77 internalization of the fluorescently labeled anandamide analog SKM 4-45-1 ([3',6'-bis(acetyloxy)-3-ox

78 t of methanandmide (5 mg/kg, i.p.), a stable anandamide analog, on the hyperthermia and hyperactivity

79 TRP channel agonists anandamide and (-)menthol were found to inhibit and acti

80 of NAPE-PLD and DAGLalpha, which synthesize anandamide and 2-AG, respectively, were elevated in the

81 The best-known endocannabinoid ligands, anandamide and 2-AG, signal at least seven receptors and

82 The endocannabinoids (eCBs) anandamide and 2-arachidonoyl glycerol (2-AG) are inacti

83 line-treated rats, and spinal cord levels of anandamide and 2-arachidonoyl glycerol (2-AG) were incre

84 The two main endogenous cannabinoids, anandamide and 2-arachidonoyl glycerol (2-AG), are produ

85 over the past decades since the discovery of anandamide and 2-arachidonoyl glycerol (2-AG).

86 xtracellular effects of the endocannabinoids anandamide and 2-arachidonoyl glycerol are terminated by

87 CB2, and the major endogenous cannabinoids (anandamide and 2-arachidonoyl glycerol) were identified

88 The levels of the endocannabinoids, anandamide and 2-arachidonoylglycerol (2-AG), and the CB

89 1Rs), and the enzymatic machinery regulating anandamide and 2-arachidonoylglycerol bioavailability.

90 nificant down-regulation of endocannabinoids anandamide and 2-arachidonoylglycerol in muscle and live

91 ow that CB1R activation by endocannabinoids (anandamide and 2-arachidonoylglycerol) or synthetic agon

92 Endocannabinoids, including anandamide and 2-arachidonoylglycerol, and the endocanna

93 The endocannabinoids anandamide and 2-arachidonoylglycerol, as well as severa

94 n the hepatic levels of the endocannabinoids anandamide and 2-arachidonoylglycerol, which originate f

95 nd inactivation of the two endocannabinoids, anandamide and 2-arachidonoylglycerol.

96 aled no clear effect of the endocannabinoids anandamide and 2-arachidonoylglycerol; however, the clas

97 functional responses to the endocannabinoids anandamide and 2-arachidonyl glycerol (2-AG), as well as

98 a G(i/o) protein inhibitor, suggesting that anandamide and 2-arachidonylglycerol did not exert their

99 rrow stromal cells express endocannabinoids (anandamide and 2-arachidonylglycerol), whereas CB recept

100 e effects of the two major endocannabinoids, anandamide and 2-arachidonylglycerol, on numerous cholan

101 Other proposed agonists of GPR18, including anandamide and abnormal cannabidiol, also failed to indu

102 y application of the endogenous cannabinoid, anandamide and blocked by VR1 antagonists.

103 We then examined the effects of anandamide and cannabidiol on peak transient and resurge

104 depression, mediated by the endocannabinoid anandamide and cannabinoid receptor 1 (CB1), was signifi

105 Finally we demonstrated that anandamide and ceramide treatment of cholangiocarcinoma

106 e biomarkers examined collectively--OMAR VT, anandamide and cortisol--correctly classified nearly 85%

107 ical data suggests that interactions between anandamide and CRF1 represent a fundamental molecular me

108 enetic background predicting relatively high anandamide and CRF1 signaling exhibited blunted basolate

109 release, in contrast, is likely mediated by anandamide and is insensitive to astrocytic buffering.

110 The biosynthetic pathway(s) for anandamide and its N-acyl ethanolamine (NAE) congeners r

111 nists including capsaicin (CAP) and the eCBs anandamide and N-arachidonoyl-dopamine elevated [Ca(2+)

112 inhibitors raise endogenous brain levels of anandamide and other FAAH substrates upon intraperitonea

113 Infusion of NAEs (anandamide and palmitoylethanolamide) recapitulated incr

114 disrupt the cellular uptake of the lipid EC anandamide and promote analgesia in vivo.

115 -domain, acid-sensitive K+ channel) blockers anandamide and quinidine.

116 which have been shown to break down the eCB anandamide and related acyl amides.

117 rolase (FAAH) hydrolyzes the endocannabinoid anandamide and related amidated signaling lipids.

118 either the 2-arachidonoylglycerol (2-AG) or anandamide and tested for changes in response to nocicep

119 Both the prototypic endocannabinoid anandamide and the CB1-selective agonist arachidonyl-2-c

120 amides including the endogenous cannabinoid anandamide and the sleep-inducing molecule oleamide.

121 ers that includes the endogenous cannabinoid anandamide and the sleep-inducing substance oleamide.

122 icantly enhance the inhibition observed with anandamide and virodhamine.

123 ccurring ligands N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), their bio

124 ological TRPV1 agonists (resiniferatoxin and anandamide) and a TRPV1 antagonist (AMG0347) confirmed t

125 ic expression of CB1R, its endogenous ligand anandamide, and a number of tumor-promoting genes, inclu

126 nd endogenous (i.e., 2-arachidonoylglycerol, anandamide, and noladin ether) CB2R ligands by competiti

127 tracellular environment, the endocannabinoid anandamide, and removal of extracellular zinc, a potent

128 e extracellular environment, endocannabinoid anandamide, and removal of extracellular zinc, a potent

129 deleting the CB1 receptor only reduces both anandamide- and capsaicin-evoked responses in ACR neuron

130 The endocannabinoid anandamide (arachidonoyl ethanolamide, AEA) is an unchar

131 The effects of the endocannabinoid anandamide (arachidonylethanolamide, AEA) on the functio

132 mical structure, 2-arachidonoyl glycerol and anandamide are synthesized and degraded by distinct enzy

133 RB597 and MAFP), but it enhanced affinity of anandamide at the CB1 receptor, thereby potentiating the

134 the myocardial level of the endocannabinoid anandamide (but not CB1/CB2 receptor expression) was ele

135 c plasticity mediated by the endocannabinoid anandamide, but not 2-arachidonoylglycerol in a mouse mo

136 In addition, anandamide, but not 2-arachidonylglycerol, induced an ac

137 clodextrin and filipin, we demonstrated that anandamide, but not 2-arachidonylglycerol, requires lipi

138 l differentiated CAD (dCAD) cells accumulate anandamide by a process that is inhibited in a dose-depe

139 Oxidation of the endocannabinoid anandamide by cytochrome P450 (P450) enzymes has the pot

140 ned, our results suggest that epoxidation of anandamide by P450s to form 5,6-EET-EA represents an end

141 Anandamide can be generated from its membrane precursor,

142 oid, previous studies have demonstrated that anandamide can excite primary sensory neurons in vitro v

143 may be the result of an accumulation of the anandamide carrier protein in detergent-resistant membra

144 r receptor type 1 (CRF1) potentiation of the anandamide catabolic enzyme fatty acid amide hydrolase.

145 nd an associated decrease in activity of the anandamide-catabolizing enzyme, fatty acid amide hydrola

146 Anandamide concentrations were reduced in the PTSD relat

147 In addition, the anandamide conjugates were found to be nontoxic.

148 ociated with visceral hyperalgesia, enhanced anandamide content, increased TRPV1, and decreased CB1 r

149 trometry was used to measure endocannabinoid anandamide content.

150 suggesting that selectively elevating brain anandamide could modulate plastic changes in fear.

151 damide internalization in vitro, interrupted anandamide deactivation in vivo and exerted profound ana

152 This enzyme is responsible for anandamide degradation and therefore has been pursued as

153 Genetic or pharmacological interruption of anandamide degradation offsets the effects of oxytocin r

154 egradation, but was unaffected by inhibiting anandamide degradation.

155 artly cytosolic variant of the intracellular anandamide-degrading enzyme fatty acid amide hydrolase-1

156 ce endocannabinoid signaling by blocking the anandamide-degrading membrane enzyme fatty acid amide hy

157 ation by capsaicin or by the endocannabinoid anandamide depresses somatic, but not dendritic inhibito

158 tamide signaling in preadipocytes is a novel anandamide-derived antiadipogenic mechanism.

159 decrease in gastrointestinal transit, while anandamide did not alter transporter-mediated glucose ab

160 rgone injury-induced sensitization, 2-AG and anandamide diminished sensitization to nociceptive stimu

161 The data indicate that, by controlling anandamide disposition and activities, FABP5 plays a key

162 ent in fear extinction reflect reductions in anandamide driven by corticotropin-releasing factor rece

163 Our findings show that augmenting amygdala anandamide enables extinction-driven reductions in fear

164 lication of the TRPV1 agonists capsaicin and anandamide evoked a transduction-like current.

165 Our results indicate that anandamide excited cutaneous C nociceptors and produced

166 the present study, we sought to determine if anandamide excited cutaneous C nociceptors in vivo and i

167 ther sodium channel inhibitors, riluzole and anandamide, exhibit differential inhibition of resurgent

168 c polymorphisms associated with differential anandamide (FAAH rs324420) and CRF1 (CRHR1 rs110402) sig

169 t mouse brain contains much higher levels of anandamide (>1 nmol/g tissue) than previously reported,

170 receptors, and blockade of the catabolism of anandamide had significantly greater inhibitory effects

171 Anandamide has been characterized as both an endocannabi

172 c cell subset expresses higher levels of the anandamide hydrolase fatty acid amide hydrolase (FAAH).

173 Systemic administration of the anandamide hydrolysis inhibitor URB597 increased social

174 in the hepatic levels of the endocannabinoid anandamide [i.e., arachidonoylethanolamide (AEA)] has be

175 Anandamide improved hyperglycemia after oral glucose cha

176 (TRPV1-LTD) mediated by the endocannabinoid anandamide in a type 1 cannabinoid receptor-independent

177 Evidence implicates anandamide in dopamine-related cocaine function.

178 onstrate that 5,6-EET-EA is more stable than anandamide in mouse brain homogenates and is primarily m

179 Along with complex I, the endocannabinoids anandamide in muscle (P = 0.003) and 2-arachidonoylglyce

180 PGF2alphaEA is produced from anandamide in preadipocytes and much less so in differen

181 inoids delta-9-tetrahydrocannabinol (THC) or anandamide in squirrel monkeys.

182 play increased levels of the endocannabinoid anandamide in the amygdala and nucleus accumbens (NAc),

183 nificant and selective increase in levels of anandamide in the BLA, and an associated decrease in act

184 n of the biosynthesis of the endocannabinoid anandamide in the liver via an in vivo pathway involving

185 or a multistep pathway for the production of anandamide in the nervous system by the sequential actio

186 MBH leptin suppresses the endocannabinoid anandamide in WAT, and, when this suppression of endocan

187 rther showed that treatment of a long-acting anandamide in wild-type mice at midgestation triggered p

188 nabinoids, 2-arachidonoylglycerol (2-AG) and anandamide, in mediating DSI.

189 endogenous marijuana-like neurotransmitter, anandamide, in the mouse nucleus accumbens (NAc), a brai

190 cifically, we find that both WIN55,212-2 and anandamide increase the frequency of miniature IPSCs (mI

191 ed mouse hepatocytes and HepG2 cells, the EC anandamide increased ceramide synthesis in an eIF2alpha-

192 The anandamide-induced calcium increase was reduced by block

193 mulation of ceramide, which was required for anandamide-induced suppression of cell growth.

194 Treatment of wild-type mice with anandamide induces similar changes mediated via activati

195 The endocannabinoid anandamide inhibits human neutrophil migration at nanomo

196 hthalazine derivative ARN272, that prevented anandamide internalization in vitro, interrupted anandam

197 Injection of anandamide into the RF dose-dependently excited nocicept

198 ibition of FABPs and subsequent elevation of anandamide is a promising new approach to drug discovery

199 Anandamide is also generated by macrophages where its en

200 Anandamide is degraded by FAAH and primarily works by ac

201 The endocannabinoid anandamide is degraded by the catabolic enzyme fatty aci

202 rminating the actions of the endocannabinoid anandamide is hydrolysis by fatty acid amide hydrolase (

203 First, they are carried into cells, and then anandamide is hydrolyzed by fatty acid amide hydrolase (

204 Anandamide is implicated in the mediation of fear behavi

205 The endocannabinoid anandamide is removed from the synaptic space by a selec

206 e endocannabinoid arachidonoyl ethanolamine (anandamide) is a lipid transmitter synthesized and relea

207 yl glycine (NAGly), a carboxylic analogue of anandamide, is an endogenous ligand of the Galpha(i/o) p

208 siological studies suggest 2-AG, rather than anandamide, is the true natural ligand for cannabinoid r

209 cortex of the rat brain and have determined anandamide level differences following the administratio

210 nder and that, depending on such parameters, anandamide levels could be underestimated.

211 r, and augmented the associated elevation in anandamide levels in the amygdala, but not the NAc.

212 Anandamide levels in the basolateral amygdala were incre

213 Anandamide levels in the nucleus accumbens (NAc) shell w

214 RB937 suppressed FAAH activity and increased anandamide levels outside the rodent CNS.

215 not loss, symptomatology; greater peripheral anandamide levels were associated with decreased attenti

216 ion-dependently reduced 2-AG levels, but not anandamide levels, in Neuro2A cells.

217 ized by increased myocardial endocannabinoid anandamide levels, oxidative/nitrative stress, activatio

218 ion and activity of FAAH, thereby increasing anandamide levels.

219 Anandamide may be converted by PTGS2 (COX2) and prostagl

220 provide evidence that the cellular uptake of anandamide may occur by a dynamin 2-dependent, caveolae-

221 The results indicate that anandamide-mediated signaling at CB1 receptors, driven b

222 These results suggest that anandamide-mediated signaling at peripheral CB receptors

223 URB597 (0.25 mg/kg, i.p.), an inhibitor of anandamide metabolism, did not alter cocaine-induced hyp

224 rolase, the enzyme primarily responsible for anandamide metabolism.

225 e 1/2 (pERK1/2), N-arachidonoylethanolamine (anandamide), methanandamide, CP55940 [2-[(1R,2R,5R)-5-hy

226 acological and genetic experiments show that anandamide mobilization and consequent activation of CB1

227 inforces parental and social bonding, drives anandamide mobilization in the NAc.

228 te, 3'-cholesterol, and, as a new entity, 3'-anandamide-modified RNA in high yields and excellent pur

229 The anandamide-modified RNA shows surprisingly high transfec

230 iffers structurally from the endocannabinoid anandamide (N-arachidonoyl ethanolamide) by a single oxy

231 Anandamide (N-arachidonoylethanolamide), a bioactive lip

232 enous ligands for cannabinoid CB1 receptors, anandamide (N-arachidonoylethanolamine) and 2-arachidono

233 Anandamide (N-arachidonoylethanolamine, AEA) is an endoc

234 e for the degradation of the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).

235 ween two canonical eCB pathways mediated via anandamide (N-arachidonylethanolamine [AEA]) and 2-arach

236 l glycine), NASer (N-arachidonoyl-l-serine), anandamide, NADA (N-arachidonoyl dopamine), NATau (N-ara

237 N-arachidonoyl dopamine (NADA), but neither anandamide nor 2-arachidonoylglycerol, reduce EC inflamm

238 Neither intraplantar injection of anandamide nor vehicle produced antinociception or hyper

239 Adverse effects of elevated levels of anandamide on these processes resulting from FAAH inacti

240 ty acid amide hydrolase-induced increases in anandamide or 2-arachidonoyl glycerol (2-AG) levels, res

241 lely on one or two endocannabinoids, such as anandamide or 2-arachidonoyl glycerol, is insufficient t

242 Researchers have debated whether anandamide or 2-arachidonyl glycerol (2-AG) is a more "i

243 FAAH inactivation yielding higher anandamide or experimentally induced higher cannabinoid

244 el monkeys that previously self-administered anandamide or nicotine under a fixed-ratio schedule with

245 The effect is likely induced by anandamide or other 'endovanilloid', suggesting activati

246 A4, and 4F2 are high-affinity, high-turnover anandamide oxygenases in vitro, forming the novel metabo

247 2) Anandamide plasma concentrations exhibited no difference

248 multiple NAPEs as substrates, including the anandamide precursor C20:4 NAPE.

249 on and measurement of GP-NAEs, including the anandamide precursor glycerophospho-N-arachidonoylethano

250 Intraplantar injection of 100 microg anandamide produced nocifensive behaviors that were atte

251 ation of hepatic CB(1)R by newly synthesized anandamide promotes liver regeneration by controlling th

252 evoked 2-arachidonoylglycerol, but not tonic anandamide, regulation of GABA synaptic inputs to magnoc

253 d 2-arachidonoylglycerol, as well as several anandamide-related N-acylethanolamines, belong to a fami

254 endocannabinoids 2-arachidonoylglycerol and anandamide, respectively.

255 al tissues and the consequent enhancement of anandamide signaling at CB1 cannabinoid receptors locali

256 These data show that increased anandamide signaling in the amygdala and NAc augments so

257 suggest that abnormal CB1 receptor-mediated anandamide signaling is implicated in the etiology of PT

258 show that exogenous THC can swamp endogenous anandamide signaling systems, thereby affecting multiple

259 al changes under either silenced or elevated anandamide signaling via CB(1).

260 levations in 2-arachidonoylglycerol, but not anandamide, significantly accelerated the temporal respo

261 hemistry and the described properties of the anandamide siRNA extend the possibilities of using siRNA

262 rect glucose administration in the duodenum, anandamide still reduced plasma glucose appearance in wi

263 Anandamide stimulates adipogenesis via CB1 receptors and

264 d not selectively target resurgent currents, anandamide strongly inhibited resurgent currents with mi

265 associated with plasma levels of leptin and anandamide, suggesting an independent role of oleoyletha

266 drolase inhibitor, which blocks breakdown of anandamide, suppressed >50% of inhibitory synapses in fe

267 demonstrates that a critical balance between anandamide synthesis by N-acylphosphatidylethanolamine-s

268 t with a specific impairment in postsynaptic anandamide synthesis in YAC128 SPN.

269 ggesting that the PLC/phosphatase pathway of anandamide synthesis may be a pharmacotherapeutic target

270 expressed at the presynaptic level by local anandamide synthesis.

271 y acid amides, including the endocannabinoid anandamide, the anti-inflammatory lipid N-palmitoyl etha

272 gnaling lipids including the endocannabinoid anandamide, the omega3-fatty acids, and the lipoamino-ac

273 hibited an increased capacity for converting anandamide to 5,6-EET-EA, which correlated with increase

274 key metabolic gatekeeper, regulating on-site anandamide tone to direct preimplantation events that de

275 and oviducts creates locally an appropriate "anandamide tone" required for normal embryo development,

276 fy FLAT as a critical molecular component of anandamide transport in neural cells and a potential tar

277 Known anandamide transport inhibitors, such as AM404 and OMDM-

278 fatty acid amide hydrolysis or by inhibiting anandamide transport, implicating involvement of the end

279 amide hydrolase-1 (FAAH-1), termed FAAH-like anandamide transporter (FLAT), that lacked amidase activ

280 hin the cell membrane revealed that although anandamide treatment had no observable effect 2-arachido

281 In the current study, we show that anandamide uptake by dCAD cells may also occur by an end

282 ious data from our laboratory indicated that anandamide uptake occurs by a caveolae-related endocytic

283 ion of human neutrophil migration induced by anandamide, virodhamine, and abnormal-CBD.

284 We also observed that endogenous cannabinoid anandamide was able to reduce hepatitis by suppressing c

285 Although anandamide was antiproliferative and proapoptotic, 2-ara

286 mined whether excitation of C nociceptors by anandamide was associated with nocifensive behaviors.

287 e calcium-mobilizing effect of intracellular anandamide was dose-dependent and abolished by pretreatm

288 lied to the RF to determine if excitation by anandamide was mediated through TRPV1 receptors.

289 ngly, although suppression of degradation of anandamide was not effective, elevating 2-arachidonoylgl

290 N-Arachidonoylethanolamine (AEA, anandamide) was the first endocannabinoid to be identifi

291 se of 2-arachidonoylglycerol (2-AG), but not anandamide, was observed during nicotine withdrawal.

292 showed that fluoxetine-induced increases in anandamide were associated with the amplification of eCB

293 Importantly, cortical levels of anandamide were not significantly affected in DAGLalpha(

294 nd circulating levels of the endocannabinoid anandamide, whereas no effect was observed in the hypoth

295 cerol (2-AG) and N-arachidonoylethanolamine (anandamide), which activate cannabinoid receptors CB1 an

296 ydrolase (FAAH) degrades the endocannabinoid anandamide, which attenuates inflammation and promotes G

297 hat degrades the other major endocannabinoid anandamide, which produced sustained analgesia without i

298 ependent mobilization of the endocannabinoid anandamide, which retrogradely suppresses GABA release f

299 competitive antagonist of the interaction of anandamide with FLAT, the phthalazine derivative ARN272,

300 LAT), that lacked amidase activity but bound anandamide with low micromolar affinity and facilitated