ライフサイエンスコーパス: endocannabinoid

1 monstrates a major immunological role for an endocannabinoid.

2 s, phospholipids, lyso-phospholipids, and an endocannabinoid.

3 hat CB2 receptors are tonically activated by endocannabinoids.

4 ble for the synthesis and degradation of the endocannabinoids.

5 ogic and pathophysiologic roles to these two endocannabinoids.

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

7 ng-term depression (LTD) was mediated by the endocannabinoid 2-arachidonoyl glycerol (2-AG) acting on

8 e show that mice with elevated levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG) are prote

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

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

11 ipase (MGL), the enzyme that deactivates the endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG), exert

12 (MGL), the primary degrading enzyme for the endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG).

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

14 In this study, we demonstrate that the endocannabinoid 2-arachidonoylglycerol (2-AG) and its re

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

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

17 sts that cocaine stimulates synthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG) in midbrai

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

19 tion to arachidonic acid, COX-2 oxidizes the endocannabinoid 2-arachidonoylglycerol (2-AG) to produce

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 n enzyme that is also known to hydrolyze the endocannabinoid 2-arachidonoylglycerol in brain.

24 ol lipase (MAGL) is the enzyme degrading the endocannabinoid 2-arachidonoylglycerol, and it is involv

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

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

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

28 ng the local abundance of its substrate, the endocannabinoid 2-arachidonyl glycerol (2-AG), and eluci

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

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

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

32 t key enzymes that synthesize or degrade the endocannabinoids 2-arachidonylglycerol (2-AG) or anandam

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

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

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

36 In the brain, endocannabinoids act via Type 1-cannabinoid receptors (C

37 expected to control the temporal profile of endocannabinoid action and may impact neuronal signaling

38 Endocannabinoid activation of cannabinoid (CB1) receptor

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

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

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

42 y acid amide hydrolase (FAAH) hydrolyzes the endocannabinoid anandamide and other N-acylethanolamines

43 In rodents, elevation of the endocannabinoid anandamide due to inhibition of fatty ac

44 The endocannabinoid anandamide is elevated in cerebrospinal

45 C385A), which metabolizes the cannabis-like endocannabinoid anandamide, and dopaminergic system, mea

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

47 cid amide hydrolase to elevate levels of the endocannabinoid anandamide, more recent efforts have foc

48 drolase (FAAH), the enzyme that degrades the endocannabinoid anandamide.

49 ns between basal serum concentrations of the endocannabinoids anandamide (AEA) and 2-arachidonylglyce

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

51 vasoactive mediator imbalance, dysregulated endocannabinoid and autonomic nervous systems and endoth

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

53 The endocannabinoid and dopaminergic systems have independen

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

55 The endocannabinoid and neurosteroid systems regulate emotio

56 g and memory tasks, and on the production of endocannabinoid and related lipids through the use of co

57 ethanolamines (NAEs) have been identified as endocannabinoids and are autocrine signals that operate

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

59 t Location tasks, and alters brain levels of endocannabinoids and related lipids.

60 e (FAAH), prolongs the regulatory effects of endocannabinoids and reverses the stress-induced anxiety

61 gh early-life stress, suggesting the role of endocannabinoids and stress to sexual differentiation of

62 Endocannabinoids and their receptors are highly abundant

63 clinical data support critical roles for the endocannabinoids and their target, the CB1 cannabinoid r

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

65 hidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic

66 ounds in its orthosteric site, including the endocannabinoids, arachidonoyl ethanolamide (anandamide)

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

68 signaling system: both phytocannabinoids and endocannabinoids are capable of binding and activating t

69 Taken together, our findings establish that endocannabinoids are directly sensed by bacteria and can

70 Endocannabinoids are host-derived lipid hormones that fu

71 Circulating endocannabinoids are stress-responsive and there is evid

72 Endogenous cannabinoids (endocannabinoids) are small molecules biosynthesized fro

73 from a postsynaptic neuron, orchestrated by endocannabinoids, astrocytic calcium signaling, and pres

74 en a surge of interest in the development of endocannabinoid-based therapeutic approaches for the tre

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

76 ession of Cb1Rs and increased degradation of endocannabinoids by monoacylglycerol lipase.

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

78 Although determination of circulating endocannabinoids can provide important information about

79 An endocannabinoid CB1 receptor-mediated suppression of GAB

80 eptor function by (i) increasing the rate of endocannabinoid clearance from the synapse and (ii) decr

81 rator-activated receptor (PPAR)-alpha by the endocannabinoid congener N-palmitoylethanolamine (PEA) r

82 ity in the adult NAc core and illustrate how endocannabinoids contribute to pathway-specific synaptic

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

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

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

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

87 d system in which GABA signaling accelerates endocannabinoid degradation, and triggers a form of lear

88 is was responsible for driving the change in endocannabinoid degradation.

89 Endocannabinoid-dependent effects of corticosterone on i

90 ood restriction and a high-fat diet cause an endocannabinoid-dependent inhibition of D1 medium spiny

91 inhibited corticostriatal transmission in an endocannabinoid-dependent manner.

92 60172) increased pyramidal output through an endocannabinoid-dependent mechanism because intracellula

93 robust antipsychotic-like effects through an endocannabinoid-dependent mechanism.

94 e show that nutritional omega-6 PUFA-derived endocannabinoids desensitize CB(1) cannabinoid receptors

95 Endocannabinoids directly activate TRPV1 and inhibit it

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

97 Conversion of omega-6 PUFAs into endocannabinoids disrupted the temporal precision of sig

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

99 2019) demonstrate a novel mechanism by which endocannabinoids drive microglia to phagocytose newborn

100 al remodeling with studies on stress-induced endocannabinoid dysregulation focusing on cerebral chang

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

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

103 The endocannabinoid (eCB) signaling system modulates neurotr

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

105 id receptors (CB(1)R), suggesting a role for endocannabinoid (eCB) signaling.

106 The endocannabinoid (eCB) system critically regulates stress

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

108 The endocannabinoid (eCB) system includes eCB compounds and

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

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

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

112 sociated with emotional disturbances and the endocannabinoid (eCB) system tunes synaptic transmission

113 The endocannabinoid (eCB) system, particularly anandamide (A

114 esistance, effects that are regulated by the endocannabinoid (eCB)/CB(1)R system.

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

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

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

118 ines (NAPEs), N-acylethanolamines (NAEs) and endocannabinoids (ECs) in 43 food products were assessed

119 We also tested the hypothesis that endocannabinoids endow excitatory circuits with pathway-

120 Both endocannabinoids enhanced responses to non-nociceptive s

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

122 The omega-3 endocannabinoid epoxides are derived from docosahexaenoi

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

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

125 may represent a potential mechanism whereby endocannabinoids exert anxiolytic and antidepressant-lik

126 t are independent of CB(1)-receptor-mediated endocannabinoid functions.

127 volves complex signaling including dopamine, endocannabinoids, GABA, and adenosine, with adenosine se

128 s open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR

129 Recently, endocannabinoids have been implicated in cardiovascular

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

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

132 The major endocannabinoid in the mammalian brain is the bioactive

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

134 lar, but not identical, to the action of NAE endocannabinoids in animal systems.

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

136 g selectively accelerates the degradation of endocannabinoids in the cerebellum.

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

141 2-arachidonoylglycerol (2-AG), the major CNS endocannabinoid, in the modulation of CSPGs deposition i

142 ovel mechanisms of brain development whereby endocannabinoids induce microglia phagocytosis to regula

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

144 Endocannabinoids inhibit GABA release in the RVM, but it

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

146 Endocannabinoid levels were measured using liquid chroma

147 and analgesic effects in mice by increasing endocannabinoid levels.

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

149 Finally, we measured brain and calvarial endocannabinoids levels post-mTBI.

150 gnaling of the most abundant and efficacious endocannabinoid ligand, 2-arachidonoylglycerol (2-AG).

151 In mammals, anandamide, as an endocannabinoid ligand, mediates several neurological an

152 The endocannabinoid-like compounds oleoylethanolamine (OEA)

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

154 This endocannabinoid-mediated depolarization-induced suppress

155 teraction between NMDA receptor-mediated and endocannabinoid-mediated forms of synaptic plasticity in

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

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

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

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

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

161 We identify the endocannabinoid-metabolizing enzyme abhydrolase domain c

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

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

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

165 xpected roles for both CCK+ interneurons and endocannabinoid modulation in hippocampal-prefrontal com

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

167 e prelimbic medial PFC, by virtue of reduced endocannabinoid modulation.

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

169 hrough complex signaling involving dopamine, endocannabinoids, neuregulin-1, GABA, and adenosine, wit

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

171 However, the effects of endocannabinoids on host susceptibility to infection has

172 The endocannabinoid palmitoylethanolamide (PEA) modified the

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

174 rane trafficking and uncovers an alternative endocannabinoid pharmacology.

175 At adult CA3-CA1 synapses, endocannabinoids play a role in this process, but how ac

176 Across many species, endocannabinoids play an important role in regulating so

177 Endocannabinoids promote energy conservation in obesity,

178 bits striatal dopamine release by mobilizing endocannabinoids, providing a mechanism for local effect

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

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

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

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

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

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

185 cts in PL-PFC networks communicating through endocannabinoid-regulated NMDA receptors.

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

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

188 postnatal day 70) cerebellar and hippocampal endocannabinoids, related lipids, and mRNA were assessed

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

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

191 n-coupled receptors (GPCRs) typically induce endocannabinoid release through activation of Galpha(q/1

192 Endocannabinoids retrogradely regulate synaptic transmis

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

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

195 vation of cerebellar Purkinje cells enhanced endocannabinoid signaling and impaired memory consolidat

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

197 ntify 2-arachidonoylglycerol (2-AG)-mediated endocannabinoid signaling as a key mechanism limiting gl

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

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

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

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

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

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

204 eveal that the synapse-specific breakdown of endocannabinoid signaling in the prelimbic prefrontal co

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

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

207 nal behavior.SIGNIFICANCE STATEMENT Amygdala endocannabinoid signaling is involved in the regulation

208 e of PirB, the NMDAR-dependent regulation of endocannabinoid signaling is lost, while CB1R-dependent

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

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

211 the well-known bioactive metabolites of the endocannabinoid signaling pathway.

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

213 crease in glycerophospholipid metabolism and endocannabinoid signaling pathways.

214 Endocannabinoid signaling plays a regulatory role in var

215 Endocannabinoid signaling plays an important role in reg

216 Enhancing endocannabinoid signaling produces anxiolytic- and antid

217 we found that 2-arachidonoylglycerol (2-AG) endocannabinoid signaling reduced BLA-NAc glutamatergic

218 nsights on the mechanisms by which amygdalar endocannabinoid signaling regulates emotional behavior.S

219 explained by the disengagement of retrograde endocannabinoid signaling selectively at excitatory syna

220 The endocannabinoid signaling system (ECSS) is altered by ex

221 Here, we show that a robust endocannabinoid signaling system modulates synaptic tran

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

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

224 Dysregulated endocannabinoid signaling was linked to inflammation and

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

226 ption is that "on-demand" release determines endocannabinoid signaling, their rapid degradation is ex

227 the behavioral significance of this MSDB-MHb endocannabinoid signaling, we induced MSDB-specific knoc

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

229 asticity and learning via activity-dependent endocannabinoid signaling.

230 ncluding regulation of insulin secretion and endocannabinoid signaling.

231 s as a key gatekeeper regulating the tone of endocannabinoid signaling.

232 MDA receptor mediated processes may suppress endocannabinoid signaling.

233 depression, and neurotrophin and retrograde endocannabinoid signaling.

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

235 One approach is to potentiate endocannabinoid signalling by inhibiting fatty acid amid

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

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

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

239 ce is controlled by the fine balance between endocannabinoid synthesis and degradation.

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

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

242 The endocannabinoid system (eCBs) encompasses the endocannab

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

244 The endocannabinoid system (ECS) is a widespread neuromodula

245 The endocannabinoid system (ECS) is considered a key player

246 ntral olfactory circuits, in tandem with the endocannabinoid system (ECS), plays a key role in mediat

247 fect many gastrointestinal processes via the endocannabinoid system (ECS).

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

249 Accordingly, the cerebellar endocannabinoid system exhibits robust sex-specific diff

250 The endocannabinoid system has been implicated in the modula

251 Through the years, the endocannabinoid system has been recognized in the homeos

252 Although studies suggest that the endocannabinoid system has immunomodulatory properties,

253 The endocannabinoid system has previously been shown to play

254 The endocannabinoid system has recently been implicated in t

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

256 Emerging evidence points to the role of the endocannabinoid system in long-term stress-induced neura

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

258 gnaling based on the fundamental role of the endocannabinoid system in synaptic plasticity and emotio

259 Our study uncovers a functional role for the endocannabinoid system in the inhibition of MC-dependent

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

261 Converging evidence suggests a role for the endocannabinoid system in these effects.

262 reciprocal interaction between GABA and the endocannabinoid system in which GABA signaling accelerat

263 The endocannabinoid system is a key regulator of the respons

264 Preclinical evidence indicates that the endocannabinoid system is involved in neural responses t

265 The endocannabinoid system is therefore a plausible target i

266 The endocannabinoid system is thought to modulate nociceptiv

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

268 The endocannabinoid system plays important roles in brain de

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

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

271 tor 55 (GPR55), a nonclassic receptor of the endocannabinoid system that is activated by L-alpha-lyso

272 Disruption of the endocannabinoid system through pharmacological or geneti

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

274 The endocannabinoid system, and in particular the cannabinoi

275 r MAGL over the other main components of the endocannabinoid system, endowed of a promising antiproli

276 research suggests its relationship with the endocannabinoid system, not only because it is able to r

277 The brain's endocannabinoid system, the primary target of cannabis,

278 drug design toward precise modulation of the endocannabinoid system.

279 tomical and functional investigations of the endocannabinoid system.

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

281 which led to the discovery of the mammalian endocannabinoid system.

282 of GPR55 and LPI being genuine actors of the endocannabinoid system.

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

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

285 Human endocannabinoid systems modulate multiple physiological

286 inergic, orexinergic, immune, melatonin, and endocannabinoid systems; the hypothalamus-pituitary-adre

287 ptor mGluR5 triggers retrograde signaling of endocannabinoids that activate presynaptic cannabinoid C

288 ific circuit control was also facilitated by endocannabinoids that endow bidirectional synaptic plast

289 the central neural effects of Delta9-THC and endocannabinoids that regulate NMDA receptor-dependent s

290 ndocannabinoid system (eCBs) encompasses the endocannabinoids, their synthetic and degradative enzyme

291 adipose tissue mass, and exaggerated hepatic endocannabinoid tone in F1 offspring exposed to 0.1 mg/k

292 Pharmacologically increasing endocannabinoid tone mimics GEE effects on cognition and

293 we report that androgen-induced increases in endocannabinoid tone promote microglia phagocytosis duri

294 from parvalbumin interneurons, and increased endocannabinoid tone.

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

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

297 e radical scavenger and an anti-inflammatory endocannabinoid, we hereby report the utility of the mod

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

299 Endocannabinoids were known to exist only among Animalia

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