ライフサイエンスコーパス: endocannabinoid

1 eta-endorphin (an opioid) and anandamide (an endocannabinoid).

2 in vitro glucocorticoid-induced, release of endocannabinoid.

3 monstrates a major immunological role for an endocannabinoid.

4 ble for the synthesis and degradation of the endocannabinoids.

5 ogic and pathophysiologic roles to these two endocannabinoids.

6 of endogenous analogues of cannabinoids, or endocannabinoids.

7 r cannabis use disorder that target FAAH and endocannabinoids.

8 pectrometry, we identify these repressors as endocannabinoids.

9 induced anxiety that relies on modulation of endocannabinoids.

10 hat CB2 receptors are tonically activated by endocannabinoids.

11 The present findings indicate that the endocannabinoid 2-AG in the hippocampus plays a key role

12 as mediated by the retrograde release of the endocannabinoid 2-AG.

13 Neuron, Gantz and Bean (2017) show that the endocannabinoid 2-arachidonoyl glycerol (2-AG) can direc

14 ects of CB2 receptor agonists, including the endocannabinoid 2-arachidonoyl glycerol (2-AG), for [35S

15 actor in the hydrolytic deactivation of the endocannabinoid 2-arachidonoyl-sn-glycerol (2AG), is tig

16 The endocannabinoid 2-arachidonoylglycerol (2-AG) has been p

17 Deficits in signaling mediated by the endocannabinoid 2-arachidonoylglycerol (2-AG) have been

18 Here, we show that alpha cells produce the endocannabinoid 2-arachidonoylglycerol (2-AG) in mouse f

19 The endocannabinoid 2-arachidonoylglycerol (2-AG) mediates r

20 Here we report that the endocannabinoid 2-arachidonoylglycerol (2-AG), via stimu

21 ent Delta(9)-tetrahydrocannabinol, i.e., the endocannabinoid 2-arachidonoylglycerol (2-AG), which act

22 mpaired retrograde synaptic signaling by the endocannabinoid 2-arachidonoylglycerol (2-AG).

23 ymes responsible for the biosynthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG).

24 e-dependent lipid hydrolase by depleting the endocannabinoid 2-arachidonoylglycerol (2AG) from plasma

25 Here we demonstrate that the endocannabinoid 2-arachidonoylglycerol in the hippocampu

26 Thus, our findings provide evidence that the endocannabinoid 2-arachidonoylglycerol is a key player i

27 nts show metabotropic glutamate receptor and endocannabinoid 2-arachidonoylglycerol-dependent plastic

28 and DAGLbeta) convert diacylglycerol to the endocannabinoid 2-arachidonoylglycerol.

29 (MAGL), the major degradative enzyme of the endocannabinoid 2-arachidonoylglycerol.

30 is required for efficient hydrolysis of the endocannabinoid 2-arachidonoylglyerol (2-AG) in the brai

31 In the healthy brain, the endocannabinoid 2-arachidonylglycerol 1) is synthesized

32 osteric modulation of mGlu5 or inhibition of endocannabinoid 2-arachidonylglycerol degradation, fully

33 The endocannabinoids 2-arachidonoyl-glycerol and N-arachidon

34 -2) oxygenates arachidonic acid (AA) and the endocannabinoids 2-arachidonoylglycerol (2-AG) and arach

35 lutamate receptor 5 (mGluR5) fails to engage endocannabinoid (2-AG) signaling to overcome abnormal sy

36 es to sweet compounds after AM251, increased endocannabinoid (2-arachidonoyl-sn-glycerol (2-AG)) leve

37 macrophages and dendritic cells produce the endocannabinoid, 2-arachidonoyl-sn-glycerol (2-AG) upon

38 elective increase in the mobilization of the endocannabinoid, 2-arachidonoyl-sn-glycerol (2-AG), in t

39 Endocannabinoid activation of cannabinoid (CB1) receptor

40 fically whether such a treatment that blocks endocannabinoid activity can induce changes in gut micro

41 ty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact th

42 t that CBD and THC elevate the levels of the endocannabinoid anandamide (AEA) when administered to hu

43 lase (FAAH), which causes a reduction in the endocannabinoid anandamide (AEA), within the amygdala.

44 (NAGly), which differs structurally from the endocannabinoid anandamide (N-arachidonoyl ethanolamide)

45 nduced long-term depression, mediated by the endocannabinoid anandamide and cannabinoid receptor 1 (C

46 echanisms for terminating the actions of the endocannabinoid anandamide is hydrolysis by fatty acid a

47 ficit in synaptic plasticity mediated by the endocannabinoid anandamide, but not 2-arachidonoylglycer

48 ase in hepatic and circulating levels of the endocannabinoid anandamide, whereas no effect was observ

49 tty acid amide hydrolase (FAAH) degrades the endocannabinoid anandamide, which attenuates inflammatio

50 24420), the primary catabolic enzyme for the endocannabinoid anandamide.

51 The extracellular effects of the endocannabinoids anandamide and 2-arachidonoyl glycerol

52 CB2 mediate the functional responses to the endocannabinoids anandamide and 2-arachidonyl glycerol (

53 inoma express elevated concentrations of the endocannabinoid, anandamide (AEA), in both their plasma

54 es that originate from the crosstalk between endocannabinoid and cytochrome P450 (CYP) epoxygenase me

55 siological effects are mediated through both endocannabinoid and epoxyeicosanoid signaling pathways.

56 concentrations comparable to those of other endocannabinoids and are expected to play critical roles

57 a- and intracellular mediators that includes endocannabinoids and brain-derived neurotrophic factor (

58 cluding elevations in DAGs and reductions in endocannabinoids and eicosanoids.

59 These data confirm that endocannabinoids and endocannabinoid-related compounds a

60 OX-2 inhibitors and block the oxygenation of endocannabinoids and in the context of advanced prostate

61 CB1 is activated by endocannabinoids and is a promising therapeutic target f

62 ed 18 prostanoids, 12 hydroxy-fatty acids, 9 endocannabinoids and N-acyl ethanolamides, and 21 non-hy

63 nabinoid receptors, endogenous cannabinoids (endocannabinoids), and the enzymes responsible for the s

64 Other conditions under which circulating endocannabinoids are altered include inflammation and pa

65 Endocannabinoids are implicated in the control of glucos

66 Endocannabinoids are involved in diverse aspects of phys

67 Our results suggest that while endocannabinoids are not required for induction of synap

68 Circulating endocannabinoids are stress-responsive and there is evid

69 Endogenous cannabinoids (endocannabinoids) are small molecules biosynthesized fro

70 jected intraperitoneally with anandamide, an endocannabinoid binding both CB1R and CB2R.

71 The pathways and enzymes involved in endocannabinoid biosynthesis thus play a major role in r

72 mer sufficient to inhibit the oxygenation of endocannabinoids but not arachidonic acid.

73 These results provide evidence that endocannabinoids can have opposing effects on nociceptiv

74 Although determination of circulating endocannabinoids can provide important information about

75 stress responses, whereas activation of the endocannabinoid CB1 receptor suppresses these responses.

76 gression, we analyzed the involvement of the endocannabinoid/CB1R system in murine and human HCC.

77 The endocannabinoid/CB1R system is up-regulated in chemicall

78 Endocannabinoids circulate in human and Drosophila lipop

79 binoids target cellular proteins involved in endocannabinoid clearance.

80 hich experiences or therapeutics that engage endocannabinoids could affect males and females differen

81 Comparisons were made with inhibitors of endocannabinoid deactivation (JZL184, URB597) or an orth

82 modulator would synergize with inhibitors of endocannabinoid deactivation and/or an orthosteric canna

83 Finally, we propose that a state of endocannabinoid deficiency could represent a stress susc

84 her pharmacological or genetic inhibition of endocannabinoid degradation in mHypoE-N41 and primary AR

85 osteric modulation of mGlu5 or inhibition of endocannabinoid degradation normalized behaviors and syn

86 Endocannabinoid-dependent effects of corticosterone on i

87 60172) increased pyramidal output through an endocannabinoid-dependent mechanism because intracellula

88 tress increases anxiety-like behavior via an endocannabinoid-dependent mechanism centered in the BLA.

89 strogen receptor alpha (ERalpha), mGluR, and endocannabinoid-dependent mechanism.

90 The results suggest that rescue of impaired endocannabinoid-dependent mGluR5 function in the mPFC ca

91 an unexpected role for beta-neurexins in the endocannabinoid-dependent regulation of neural circuits.

92 is study reveals that progesterone-activated endocannabinoid depletion by ABHD2 is a general mechanis

93 Endocannabinoids directly activate TRPV1 and inhibit it

94 All tested ligands, and in particular the endocannabinoids, displayed distinct kinetic profiles, s

95 duced by direct epoxygenation of the omega-3 endocannabinoids, docosahexanoyl ethanolamide (DHEA) and

96 Endocannabinoid (EC) signaling mediates psychotropic eff

97 ays, including the functional segregation of endocannabinoid (eCB) biosynthetic enzymes diacylglycero

98 compared the effect of the inhibition of the endocannabinoid (eCB) degradation versus synthetic CB ag

99 diating adolescent behavior because enhanced endocannabinoid (eCB) signaling has been suggested to oc

100 inhibition was preferentially suppressed by endocannabinoid (eCB) signaling, whereas MSN-mediated la

101 The endocannabinoid (eCB) system critically regulates stress

102 The endocannabinoid (eCB) system has emerged as a pivotal pa

103 The endocannabinoid (eCB) system has emerged as one of the m

104 suggest the presence of abnormalities in the endocannabinoid (eCB) system in schizophrenia (SCZ).

105 The endocannabinoid (eCB) system includes eCB compounds and

106 The endocannabinoid (eCB) system is a critical modulator of

107 A growing body of work indicates that the endocannabinoid (eCB) system is an integral regulator of

108 The endocannabinoid (eCB) system regulates DA release and is

109 ioid mechanisms (for example, dopamine (DA), endocannabinoids (eCB)) have been implicated in the form

110 Endocannabinoids (eCBs) exert major control over neurona

111 Pharmacologically elevating brain endocannabinoids (eCBs) share anxiolytic and fear extinc

112 While endocannabinoids (eCBs) that potentially contribute to a

113 Furthermore, TRPV1's response to endocannabinoids (eCBs), the putative endogenous retinal

114 Fatty acid ethanolamides (FAEs) and endocannabinoids (ECs) have been shown to alleviate pain

115 of GABA release is lower and that opioid and endocannabinoid effects are more evident in adult rats (

116 Opposing the action of leptin, endocannabinoids enhance sweet taste responses.

117 Both endocannabinoids enhanced responses to non-nociceptive s

118 Furthermore the omega-3 endocannabinoid epoxides 17,18-EEQ-EA and 19,20-EDP-EA e

119 The omega-3 endocannabinoid epoxides are derived from docosahexaenoi

120 In summary, the omega-3 endocannabinoid epoxides are found at concentrations com

121 Taken together, the omega-3 endocannabinoid epoxides' physiological effects are medi

122 Two main approaches to the modulation of endocannabinoid functioning have been chosen so far.

123 Interactions between the endocannabinoid, gamma-aminobutyric acid, and glutamate

124 Recently, endocannabinoids have been implicated in cardiovascular

125 However, there is evidence that endocannabinoids have both pro- and anti-nociceptive eff

126 Here we examined whether endocannabinoids have similar bidirectional effects on b

127 The major endocannabinoid in the mammalian brain is the bioactive

128 ocial use of cannabis and the involvement of endocannabinoids in a multitude of biological processes,

129 ar signaling that links ERalpha, mGluRs, and endocannabinoids in females and identify where in this p

130 udies in which concentrations of circulating endocannabinoids in humans have been examined in relatio

131 er, potential roles of endogenous leptin and endocannabinoids in sweet taste remain unclear.

132 Potential roles of endogenous leptin and endocannabinoids in sweet taste were examined by using p

133 ed expression of a biosynthesizing enzyme of endocannabinoids in taste cells.

134 ing, possibly due to increased production of endocannabinoids in taste tissue.

135 rticoids stimulate the rapid mobilization of endocannabinoids in the basolateral amygdala (BLA).

136 s (CB1Rs) mediate the presynaptic effects of endocannabinoids in the central nervous system (CNS) and

137 of postsynaptic, cell-autonomous actions of endocannabinoids in the mammalian brain.

138 The roles of endocannabinoids in the regulation of energy intake and

139 These results highlight a role for endocannabinoids in vision and present a novel mechanism

140 ed in the vertebrate retina, but the role of endocannabinoids in vision is not fully understood.

141 noid system and suggest that manipulation of endocannabinoids in vivo could affect physiological and

142 le for 2-arachidonoylglycerol, the major CNS endocannabinoid, in the modulation of chondroitin sulfat

143 2-arachidonoylglycerol (2-AG), the major CNS endocannabinoid, in the modulation of CSPGs deposition i

144 Endocannabinoids, including anandamide and 2-arachidonoy

145 one "set the stage" for relapse by promoting endocannabinoid-induced attenuation of inhibitory transm

146 Endocannabinoids inhibit GABA release in the RVM, but it

147 Endocannabinoids interact with hepatic cannabinoid 1 rec

148 balance signals such as adiponectin, apelin, endocannabinoids, leptin, insulin and peptide YY.

149 exert a negative regulation on hypothalamic endocannabinoid levels and hence on cannabinoid CB1 rece

150 to n-3 FA at a young age may decrease tissue endocannabinoid levels and prevent metabolic disorders i

151 Second, the modulation of endocannabinoid levels by use of the phytocannabinoid ca

152 ssess the behavioral consequences of reduced endocannabinoid levels in the brain.

153 lactation in mice, which permanently reduces endocannabinoid levels in the offspring, phenocopies CB1

154 es to sweet compounds after AM251, increased endocannabinoid levels in the taste organ, and enhanced

155 Endocannabinoid levels were decreased within the BLA dur

156 Endocannabinoid levels were measured using liquid chroma

157 arly diet induces a marked decrease in liver endocannabinoid levels.

158 ditions accompanied by elevated hypothalamic endocannabinoid levels.

159 and analgesic effects in mice by increasing endocannabinoid levels.

160 The endocannabinoid-like compounds oleoylethanolamine (OEA)

161 otency of GLP-1 by physiologically regulated endocannabinoid-like lipids allows GLP-1R signaling to b

162 t exendin 4, is specifically enhanced by the endocannabinoid-like lipids oleoylethanolamide (OEA) and

163 achidonyl ethanolamide (anandamide), a major endocannabinoid lipid mediator, were more susceptible to

164 lator for sweet taste in lean mice; however, endocannabinoids may become more effective modulators of

165 ggest that circulating leptin, but not local endocannabinoids, may be a dominant modulator for sweet

166 nock-out mice, and independent of opioid and endocannabinoid mechanisms.

167 gest that the emergence of habits depends on endocannabinoid-mediated attenuation of a competing circ

168 n vivo knockout of beta-neurexins aggravated endocannabinoid-mediated inhibition of synaptic transmis

169 s study, we investigated the effect of PE on endocannabinoid-mediated long-term depression (eCB-LTD)

170 addition, we found that resveratrol blocked endocannabinoid-mediated long-term synaptic depression i

171 el a previously unsuspected role for OX-A in endocannabinoid-mediated promotion of appetite by combin

172 tudy describes suitable inhibitors to target endocannabinoid membrane trafficking and uncovers an alt

173 by enhancing the production of lipid-derived endocannabinoid messengers in the gut.

174 ing receptors and the enzymatic machinery of endocannabinoid metabolism exhibit a cellular distributi

175 105 did not affect other enzymes involved in endocannabinoid metabolism including abhydrolase domain-

176 We found that endocannabinoid/mGlu5-mediated LTD and NMDAR-dependent L

177 Importantly, we discovered that endocannabinoid/mGlu5-mediated LTD in the mPFC and accum

178 As E2 has been implicated in endocannabinoid mobilization, which can disinhibit PrL-P

179 n modulatory system and an important site of endocannabinoid modulation of pain.

180 The stress-induced endocannabinoid modulation of synaptic transmission in t

181 as biosynthetic and catabolic enzymes of the endocannabinoids N-arachidonoylethanolamine and 2-arachi

182 We assessed the profiles of eicosanoids, endocannabinoids, N-acyl ethanolamides, and sphingolipid

183 The biosynthesis of the two main endocannabinoids, N-arachidonoylethanolamine and 2-arach

184 In experiments to determine the effects of endocannabinoids on animals that had undergone injury-in

185 e statement: Somatodendritic signaling using endocannabinoids or nitric oxide to alter the efficacy o

186 The endocannabinoid palmitoylethanolamide (PEA) modified the

187 or peptide of a family of endogenous peptide endocannabinoids (pepcans) shown to act as negative allo

188 rane trafficking and uncovers an alternative endocannabinoid pharmacology.

189 des suggesting that both exocannabinoids and endocannabinoids play a role in the pathophysiology of s

190 l et al. (2016) describe a mechanism whereby endocannabinoid production leads to a cell-intrinsic hyp

191 eversibly blocked membrane transport of both endocannabinoids, providing mechanistic insights into th

192 ncoding is dependent on both the LPP and the endocannabinoid receptor CB1, and is strikingly impaired

193 ff-targets: dopamine receptor subtype D2 and endocannabinoid receptor CB1.

194 hibitor, which are thought to function as an endocannabinoid receptor.

195 tion (iLTD) as a result of activation of CB1 endocannabinoid receptors on cholecystokinin-expressing

196 Specifically, the main adenosine and endocannabinoid receptors present in the striatum, ie, a

197 cause the activation of HSC is controlled by endocannabinoid receptors, CB-1 and CB-2, the mice recei

198 Endocannabinoids regulate brain development via modulati

199 Moreover, in some cell niches, endocannabinoids regulate cell proliferation, fate deter

200 d receptor agonists as well as inhibitors of endocannabinoid-regulating enzymes fatty acid amide hydr

201 rate the analgesic efficacy of inhibitors of endocannabinoid-regulating enzymes.

202 We tested for rapid glucocorticoid-induced endocannabinoid regulation of synaptic inhibition in the

203 These data confirm that endocannabinoids and endocannabinoid-related compounds are involved in food-r

204 andamide and 2-arachidonoylglycerol, and the endocannabinoid-related compounds oleoylethanolamide and

205 ic inhibition that is mediated by retrograde endocannabinoid release at GABA synapses.

206 es with no effect in males, indicating tonic endocannabinoid release in females that is absent in mal

207 Activity-dependent endocannabinoid release may modulate signal gain in RGCs

208 hesis inhibition, which impairs postsynaptic endocannabinoid release.

209 explain the increased circulating levels of endocannabinoids reported after consumption of cannabino

210 eceptors by the acetaminophen metabolite and endocannabinoid reuptake inhibitor AM 404.

211 Interestingly, increased endocannabinoid signaling activated MAPK p38, but not p4

212 Restoring endocannabinoid signaling allows mGluR5 activation to in

213 l synaptic inhibition in pain, but restoring endocannabinoid signaling allows mGluR5 to increase mPFC

214 sly unknown molecular properties controlling endocannabinoid signaling and cannabis-induced cognitive

215 ide important information about the state of endocannabinoid signaling and thus allow for hypotheses

216 hydrolase and is believed to play a role in endocannabinoid signaling as well as in the pathogenesis

217 Conversely, we suggest that endocannabinoid signaling can be an appealing druggable

218 m of this study was to determine the role of endocannabinoid signaling in glucocorticoid-mediated obe

219 tropic glutamate receptor subtype mGluR5 and endocannabinoid signaling in infralimbic pyramidal cells

220 emergent insight from these studies is that endocannabinoid signaling in specific circuits of the br

221 triggers long-term changes in 2-AG-mediated endocannabinoid signaling in the amygdala, and that phar

222 creased in diabetic mice, indicating reduced endocannabinoid signaling in the diabetic heart.

223 understand the role of coordinated adenosine-endocannabinoid signaling in the indirect striatal pathw

224 The contributions of endocannabinoid signaling in the PL to the effects of st

225 ned consistently support the hypothesis that endocannabinoid signaling is associated with increased c

226 These results provide evidence that endocannabinoid signaling is critical in regulating deci

227 Given that endocannabinoid signaling is thought to exert "tonic" re

228 A second important role for endocannabinoid signaling is to restore homeostasis foll

229 lizing enzyme of 2-arachidonoyl glycerol, an endocannabinoid signaling lipid whose elevation through

230 Therefore, enhancing Galphai/o-biased endocannabinoid signaling may be therapeutically benefic

231 a unique junction between the eicosanoid and endocannabinoid signaling pathways.

232 Endocannabinoid signaling plays an important role in reg

233 entrally in the manifestation of stress, and endocannabinoid signaling reduces the activity of hypoth

234 We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphi

235 n of presynaptic CB1 receptors by retrograde endocannabinoid signaling stimulates protein synthesis i

236 models have revealed important roles for the endocannabinoid signaling system, comprising G protein-c

237 CE STATEMENT: These studies demonstrate that endocannabinoid signaling to CB1 and CB2 receptors in ad

238 In particular, indirectly enhancing endocannabinoid signaling to therapeutic levels through

239 arked by dynamic changes in gene expression, endocannabinoid signaling, and frontolimbic circuitry.

240 However, the mechanisms involving endocannabinoid signaling, glucose uptake, and IR in car

241 eceptor inhibition, which blocks presynaptic endocannabinoid signaling, or by 2-arachidonoylglycerol

242 ment terms morphine addiction and retrograde endocannabinoid signaling, whereas binge eating resulted

243 cocorticoids possess the ability to increase endocannabinoid signaling, which is known to regulate ap

244 depression, and neurotrophin and retrograde endocannabinoid signaling.

245 thways including lipids, Kynurenine pathway, endocannabinoids signaling pathway and the RNA editing p

246 blocking activation of endogenous leptin and endocannabinoid signalling on taste responses in lean co

247 the oxygenation of arachidonic acid (AA) and endocannabinoid substrates, placing the enzyme at a uniq

248 ctions, the impact of cyclooxygenase-derived endocannabinoids such as PGE2-EA or PGE2-G on neutrophil

249 The rapid glucocorticoid-induced endocannabinoid suppression of synaptic inhibition is in

250 The endocannabinoid system (eCB) is implicated in the mediat

251 ity is associated with increased activity of endocannabinoid system (eCB).

252 Over recent years, the interest in the endocannabinoid system (ECS) as a new target for the tre

253 The endocannabinoid system (ECS) consists of the naturally o

254 The endocannabinoid system (ECS) is a widespread neuromodula

255 The endocannabinoid system (ECS) is associated with an alter

256 Drugs acting on the endocannabinoid system and genetically modified mice wer

257 pendent and E2-independent regulation of the endocannabinoid system and suggest that manipulation of

258 simultaneously target the recently proposed endocannabinoid system and the classic cholinesterase sy

259 nteractions between these alterations in the endocannabinoid system and those in other inhibitory neu

260 These findings implicate the endocannabinoid system as a notable research target for

261 The endocannabinoid system comprises cannabinoid receptors 1

262 Our finding that molecular regulation of the endocannabinoid system differs between the sexes suggest

263 The endocannabinoid system has an important role in formatio

264 The endocannabinoid system has been implicated in the modula

265 The endocannabinoid system has previously been shown to play

266 The endocannabinoid system has recently been implicated in t

267 Recent studies find impairment of the endocannabinoid system in animal models but the function

268 Our study unveils a role for the endocannabinoid system in maintaining immune homeostasis

269 like behavior to investigate the role of the endocannabinoid system in the development of persistent

270 te memories through the dysregulation of the endocannabinoid system in the PFC.

271 We thus demonstrate that the endocannabinoid system is crucial for two main aspects o

272 The modulation of the endocannabinoid system is emerging as a viable avenue fo

273 The endocannabinoid system is thought to modulate nociceptiv

274 Alterations in the endocannabinoid system may profoundly dysregulate develo

275 ere, we investigated whether the hippocampal endocannabinoid system modulates memory retrieval depend

276 The endocannabinoid system negatively regulates the release

277 lterations in the maturational events of the endocannabinoid system occurring in the adolescent brain

278 on of whether pharmacotherapies aimed at the endocannabinoid system promote opioid-sparing effects in

279 therapeutic option is thus required, and the endocannabinoid system provides a good candidate target.

280 preclinical and clinical evidence of various endocannabinoid system targets as potential therapeutic

281 Disruption of the endocannabinoid system through pharmacological or geneti

282 analyzed expression of genes related to the endocannabinoid system via real-time polymerase chain re

283 tivity produced a selective overdrive of the endocannabinoid system within the PFC, but not in the st

284 The endocannabinoid system, and in particular the cannabinoi

285 ulation of a key neuromodulatory system, the endocannabinoid system, in the hippocampus.

286 tomical and functional investigations of the endocannabinoid system.

287 has been proposed as a novel receptor of the endocannabinoid system.

288 en that the endogenous cannabinoid (that is, endocannabinoid) system modulates neuronal and immune ce

289 t studies suggest that the glutamatergic and endocannabinoid systems exhibit a functional interaction

290 ave implicated the cholecystokinin (CCK) and endocannabinoid systems in fear; however, there is a hig

291 Overall, our data mechanistically link endocannabinoids to cell proliferation and sorting durin

292 n alternative strategy to drugs for reducing endocannabinoid tone and improving metabolic parameters

293 in, 3) blunted under conditions of increased endocannabinoid tone due to either pharmacological or ge

294 RVM neurons suggesting the presence of local endocannabinoid tone in mature RVM.

295 initially offset by a transient increase in endocannabinoid tone, but lasts days after an initial 24

296 obesity are associated with the elevation of endocannabinoid tone.

297 lack of potent and selective inhibitors for endocannabinoid transport has prevented the molecular ch

298 stituted 2,4-dodecadienamides as a selective endocannabinoid uptake inhibitor.

299 using Hirudo verbana (the medicinal leech), endocannabinoids were found to depress nociceptive synap

300 Physical exercise mobilizes endocannabinoids, which could contribute to refilling of