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 tion produced a 10-fold increase in baseline anandamide.

4 tsynaptic endocannabinoid release, likely of anandamide.

5 ees C and pH 8.0, with higher specificity to anandamide.

6 sient receptor potential vanilloid 1 agonist anandamide.

7 e endocannabinoids 2-arachidonoylglycerol or anandamide.

8 ncreases tissue levels of the endovanilloid, anandamide.

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

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

11 ability and actions may differ from those of anandamide.

12 firing facilitated uptake and degradation of anandamide.

13 e for the degradation of the endocannabinoid anandamide.

14 nuated the excitation produced by 100 microg anandamide.

15 the enzyme that degrades the endocannabinoid anandamide.

16 an be regulated by inflammation products and anandamide.

17 oxidative metabolism of the endocannabinoid anandamide.

18 ch could be influenced by the basal level of anandamide.

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

20 t also a reduction in cortical and amygdalar anandamide.

21 ary catabolic enzyme for the endocannabinoid anandamide.

22 elay of plasma glucose appearance induced by anandamide.

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

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

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

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

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

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

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

30 atment of dCAD cells significantly inhibited anandamide accumulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

44 serum concentrations of the endocannabinoids anandamide (AEA) and 2-arachidonylglycerol (2-AG) with b

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

46 Anandamide (AEA) and other bioactive N-acylethanolamines

47 hydrolase (FAAH) produces elevated levels of anandamide (AEA) and promotes fear extinction, suggestin

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

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

50 Anandamide (AEA) content was downregulated after repeate

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

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

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

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

55 Anandamide (AEA) is an endogenous intestinal cannabinoid

56 Anandamide (AEA) is an endogenous ligand of cannabinoid

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

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

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

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

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

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

63 Increased anandamide (AEA) signaling through inhibition of its cat

64 e endocannabinoid (eCB) system, particularly anandamide (AEA) signaling, controls neuronal excitabili

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

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

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

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

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

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

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

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

73 adation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-ole

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

75 ellular transporters for the endocannabinoid anandamide (AEA).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 1Rs), and the enzymatic machinery regulating anandamide and 2-arachidonoylglycerol bioavailability.

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

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

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

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

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

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

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

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

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

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

106 Finally we demonstrated that anandamide and ceramide treatment of cholangiocarcinoma

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

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

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

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

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

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

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

114 rolase (FAAH) hydrolyzes the endocannabinoid anandamide and other N-acylethanolamines.

115 Infusion of NAEs (anandamide and palmitoylethanolamide) recapitulated incr

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 icantly enhance the inhibition observed with anandamide and virodhamine.

122 endocannabinoids, arachidonoyl ethanolamide (anandamide) and 2-arachidonoyl glycerol, and the plant-d

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 etabolizes the cannabis-like endocannabinoid anandamide, and dopaminergic system, measured by dopamin

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

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

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

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

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

132 cannabinoids 2-arachidonylglycerol (2-AG) or anandamide are expressed in the MHb and MSDB, and that c

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

134 In mammals, anandamide, as an endocannabinoid ligand, mediates sever

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

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

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

138 und that mTBI resulted in elevated levels of anandamide, but not 2-arachidonoylglycerol, in the contr

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

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

141 response in the skull, probably mediated by anandamide, but seemingly unrelated to inflammation.

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

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

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

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

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

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

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

149 , and corroborated by corresponding drug and anandamide concentrations in blood.

150 Anandamide concentrations were reduced in the PTSD relat

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

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

153 trometry was used to measure endocannabinoid anandamide content.

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

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

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

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

158 egradation, but was unaffected by inhibiting anandamide degradation.

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

160 Acute pharmacological inhibition of the anandamide-degrading enzyme, fatty acid amide hydrolase

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

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

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

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

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

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

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

168 In rodents, elevation of the endocannabinoid anandamide due to inhibition of fatty acid amide hydrola

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

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

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

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

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

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

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

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

177 Anandamide has been characterized as both an endocannabi

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

179 een previously documented with inhibition of anandamide hydrolysis in the same brain region.

180 Systemic administration of the anandamide hydrolysis inhibitor URB597 increased social

181 indicate that viral-mediated augmentation of anandamide hydrolysis within the basolateral amygdala re

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

183 Anandamide improved hyperglycemia after oral glucose cha

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

185 Evidence implicates anandamide in dopamine-related cocaine function.

186 AAH mutants of moss to elucidate the role of anandamide in early land plants.

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

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

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

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

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

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

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

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

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

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

197 LEI-301 reduced the NAE levels, including anandamide, in cells overexpressing PLAAT2 or PLAAT5.

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

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

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

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

202 The anandamide-induced calcium increase was reduced by block

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

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

205 The endocannabinoid anandamide inhibits human neutrophil migration at nanomo

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

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

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

209 Anandamide is degraded by FAAH and primarily works by ac

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

211 The endocannabinoid anandamide is elevated in cerebrospinal fluid of patient

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

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

214 Anandamide is implicated in the mediation of fear behavi

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

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

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

218 We recently reported that elevated anandamide levels in people homozygous for a loss-of-fun

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

220 Anandamide levels in the basolateral amygdala were incre

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

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

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

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

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

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

227 y acid amide hydrolase (FAAH) controls brain anandamide levels; however, it is unknown if FAAH is alt

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

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

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

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

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

233 rolase, the enzyme primarily responsible for anandamide metabolism.

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

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

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

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

238 The anandamide-modified RNA shows surprisingly high transfec

239 ase to elevate levels of the endocannabinoid anandamide, more recent efforts have focused on inhibiti

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

241 Anandamide (N-arachidonoylethanolamide), a bioactive lip

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

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

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

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

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

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

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

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

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

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

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

253 2) Anandamide plasma concentrations exhibited no difference

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

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

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

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

258 endocannabinoids 2-arachidonoylglycerol and anandamide, respectively.

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

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

261 Modulation of anandamide signaling is a current clinical therapeutic t

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

263 fully understanding the mechanisms by which anandamide signaling regulates amygdala-dependent change

264 Our results indicate that the ability of anandamide signaling to regulate emotional behavior is n

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

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

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

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

269 Anandamide stimulates adipogenesis via CB1 receptors and

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

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

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

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

274 expressed at the presynaptic level by local anandamide synthesis.

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

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

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

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

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

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

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

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

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

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

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

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

291 Higher levels of anandamide were associated with greater attenuation in b

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