ライフサイエンスコーパス: CB1 receptor

1 semble those observed in animals lacking the CB1 receptor.

2 did not display affinity for the cannabinoid CB1 receptor.

3 to modulate the pharmacologically important CB1 receptor.

4 pasticity via action on the peripheral nerve CB1 receptor.

5 in HEK293 cells and rat brain expressing the CB1 receptor.

6 hile enhancing [(3)H]CP55,940 binding to the CB1 receptor.

7 ve improved affinity and selectivity for the CB1 receptor.

8 ynthesized and assessed for allostery of the CB1 receptor.

9 ry targeting the pharmacologically important CB1 receptor.

10 of Delta(9)-tetrahydrocannabinol through the CB1 receptor.

11 ylglycerol (2-AG) that activates cannabinoid CB1 receptor.

12 nted by systemic or BLA-specific blockade of CB1 receptors.

13 by pharmacological or genetic inhibition of CB1 receptors.

14 ptic strengths via presynaptically-expressed CB1 receptors.

15 fects of JZL184 were mediated by cannabinoid CB1 receptors.

16 king, both tightly controlled by cannabinoid CB1 receptors.

17 known GPCRs such as the alpha2, GABA(B), and CB1 receptors.

18 -administration and is tightly controlled by CB1 receptors.

19 d withdrawal signs in mice via activation of CB1 receptors.

20 effects are related to local availability of CB1 receptors.

21 raphy and [(18)F]FMPEP-d2, a radioligand for CB1 receptors.

22 through antagonism of peripherally expressed CB1 receptors.

23 c transmission via presynaptically expressed CB1 receptors.

24 7 nM), and moderate to good selectivity over CB1 receptors.

25 e allosteric modulators (NAM) of cannabinoid CB1 receptors.

26 e similarly modulated by activation of these CB1 receptors.

27 he synapse and (ii) decreasing expression of Cb1 receptors.

28 ormation in the femur via the cannabinoid-1 (CB1) receptor.

29 ownregulation or loss of cannabinoid type 1 (CB1) receptors.

30 enzyme diacylglycerol lipase or blockade of CB1 receptors abolished the facilitatory effect of VU036

31 d peripheral blockade of cannabinoid type-1 (CB1) receptors abolished the stress-induced memory impai

32 A selective agonist of the CB1 receptors, ACEA, up-regulates Egr1 mRNA, but does no

33 ike behavior that was attenuated by blocking CB1 receptor activation and inhibiting 2-AG synthesis in

34 CB1 receptor activation in the vlPAG attenuated dural-ev

35 ass unwanted central effects associated with CB1 receptor activation.

36 211 did not produce cardinal signs of direct CB1-receptor activation in the presence or absence of pa

37 Cardinal signs of direct CB1-receptor activation were evaluated together with the

38 ocannabinoid levels and hence on cannabinoid CB1 receptor activity.

39 binoids suppress RMTg inputs to DA cells and CB1 receptors affect alcohol intake in rodents, we hypot

40 dy was designed to determine the impact of a CB1 receptor agonist (WIN) during specific windows of ad

41 Pretreatment with G(o/i)-coupled CB1 receptor agonist attenuated subsequent FGF activatio

42 nd to be a remarkably potent and efficacious CB1 receptor agonist with relatively fast onset/offset o

43 se-dependent fashion; while lower doses of a CB1 receptor agonist, WIN 55,212-2, significantly increa

44 tively analysed the efficacy and safety of a CB1-receptor agonist administered in six patients with r

45 ntravenously self-administer the cannabinoid CB1-receptor agonist WIN55,212-2.

46 iments key analogues were shown to be potent CB1 receptor agonists and to exhibit CB1-mediated hypoth

47 In summary, CNS-excluded CB1 receptor agonists are a novel class of therapeutic a

48 nthesis, and it was mimicked and occluded by CB1 receptor agonists, indicating it was mediated by the

49 -1 (4) has generated significant interest in CB1 receptor allosteric modulation.

50 Deleting the CB1 receptor also reduces the proportion of ACR neurons

51 imonabant treatment, suggesting that central CB1 receptors also participate in the signaling pathway

52 0, 7.7 +/- 0.1) and a partial agonist at the CB1 receptor, although with a decrease in functional res

53 ed a ternary complex structural model of the CB1 receptor and Gi heterotrimer (CB1-Gi), guided by the

54 its similarity in amino acid sequence to the CB1 receptor and helped provide an explanation for the e

55 to compounds having excellent potency at the CB1 receptor and high levels of agonism, good physical a

56 d a diverse range of kinetic profiles at the CB1 receptor and their structure-kinetic relationships (

57 We suggest that spatial distribution of the CB1 receptor and TRPV1 contributes to the complexity of

58 We report that PSN co-expressing CB1 receptor and TRPV1 form two distinct sub-populations

59 sion of inhibition was prevented by blocking CB1 receptors and 2-arachidonoylglycerol (2-AG) synthesi

60 t RMTg afferents onto VTA DA neurons express CB1 receptors and display a 2-arachidonoylglycerol (2-AG

61 Anandamide stimulates adipogenesis via CB1 receptors and peroxisome proliferator-activated rece

62 LTD by reducing the function of presynaptic CB1 receptors and reveal a novel mechanism by which nora

63 -AG), via stimulation of cannabinoid type 1 (CB1) receptor and Ca(2+)/calmodulin-dependent protein ki

64 The cannabinoid type 1 (CB1) receptor and the capsaicin receptor (TRPV1) exhibit

65 tington disease, upon (i) fully knocking out CB1 receptors, and (ii) deleting CB1 receptors selective

66 rain, which is clearly distinct from that of CB1 receptors, and thus, will help us to understand bett

67 wnregulation of cannabinoid receptor type 1 (CB1) receptors, and impaired neurite outgrowth.

68 Both CB1 receptor antagonism and agonism, in particular by 2-

69 ediated modulation was inhibited by specific CB1 receptor antagonism, given via the vlPAG, and with a

70 nce, this cellular adaptation was blocked by CB1 receptor antagonism.

71 imilarly, a neutral, peripherally restricted CB1 receptor antagonist (AM6545) was able to attenuate t

72 idated auditory fear memory, by infusing the CB1 receptor antagonist AM251, or the FAAH inhibitor URB

73 ptor as well as mice treated with the global CB1 receptor antagonist AM251.

74 were blocked by intra-amygdala infusion of a CB1 receptor antagonist and were fully recapitulated by

75 biting Smoothened (Smo), while Shh mRNA or a CB1 receptor antagonist attenuated CB-induced birth defe

76 imaging scan and a resting PET scan with the CB1 receptor antagonist radiotracer [(11)C]OMAR, which m

77 ver, WIN55212 inhibition was reversed by the CB1 receptor antagonist rimonabant in naive rats but not

78 Accordingly, local injection of the CB1 receptor antagonist rimonabant into the rostral vent

79 kade, we combined the acute injection of the CB1 receptor antagonist rimonabant with the use of condi

80 wever, to date, the only clinically approved CB1 receptor antagonist, rimonabant, was withdrawn becau

81 rimonabant and 14g, a potent brain penetrant CB1 receptor antagonist, significantly reduced the rate

82 CB1 receptor antagonist-induced hypophagia was fully abo

83 , we conclude that the metabolic benefits of CB1 receptor antagonists are primarily centrally mediate

84 Peripherally restricted CB1 receptor antagonists may be useful in treating metab

85 systemic or the intra-VTA administration of CB1 receptor antagonists on running behavior were abolis

86 koxy-5-aryl-3-pyridinecarboxamides as potent CB1 receptor antagonists with high selectivity over CB2

87 dazol-4-carboxamide derivatives developed as CB1 receptor antagonists.

88 Cannabinoid type-1 (CB1) receptor antagonists are potent hypophagic agents,

89 ic transmission and blocked LTP; presynaptic CB1-receptor antagonists or postsynaptic 2-arachidonoylg

90 Type 1 cannabinoid (CB1 ) receptors are widely distributed in the brain.

91 CB1 receptors are also part of the brain endocannabinoid

92 Here, we tested whether GPR55 and CB1 receptors are capable of (i) forming heteromers and

93 Of note, CB1 receptors are expressed at the synapses of two oppos

94 ken together, these results demonstrate that CB1 receptors are functionally expressed by KCs in vivo

95 Although early studies show that CB1 receptors are present in the nervous system and CB2

96 ovide ultrastructural evidence that cortical CB1 receptors are strategically positioned for integrati

97 Given that mu opioid (MOP) and canabinoid (CB1) receptors are colocalized in various regions of the

98 potentiated binding of [(3)H]CP55,940 to the CB1 receptor as well as enhancing AEA-stimulated [(35)S]

99 or reversed in mice lacking the cannabinoid CB1 receptor as well as mice treated with the global CB1

100 ctivation and partial desensitization of the CB1 receptor at PF-PC synapses.

101 ed the cellular and molecular mechanisms how CB1 receptors attenuate CHS responses to 2,4-dinitrofluo

102 to threat mediated the relationship between CB1 receptor availability in the amygdala and severity o

103 Results revealed that increased CB1 receptor availability in the amygdala was associated

104 hese effects were positively correlated with CB1 receptor availability in the right amygdala.

105 ume of distribution (VT) linearly related to CB1 receptor availability.

106 between in vivo cannabinoid receptor type 1 (CB1) receptor availability in the amygdala, and performa

107 erse psychotropic effects that can accompany CB1 receptor-based therapies.

108 s, C allele carriers at rs2023239 had higher CB1 receptor binding compared with non-carriers.

109 d with a widespread reduction of cannabinoid CB1 receptor binding in the human brain and this reducti

110 After 2-4 weeks of abstinence, CB1 receptor binding remained similarly reduced in these

111 On the first scan, CB1 receptor binding was 20-30% lower in patients with a

112 AN(THC) administration decreased hippocampal CB1 receptor binding.

113 f their site of origin, important effects of CB1 receptor blockade are expressed via activation of pe

114 studies demonstrate for the first time that CB1 receptor blockade attenuates DIO-associated inflamma

115 -cell function independent of weight loss or CB1 receptor blockade in the brain, suggesting that peri

116 tible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previo

117 transmission also blunted central effects of CB1 receptor blockade, such as fear responses and anxiet

118 chanisms underlying the hypophagic effect of CB1 receptor blockade, we combined the acute injection o

119 ient-specific component acutely regulated by CB1 receptor blockade.

120 in, suggesting that peripherally-acting only CB1 receptor blockers may be useful therapeutic agents.

121 al use of first-generation, centrally acting CB1 receptor blockers.

122 tion to determine the structure of the human CB1 receptor bound to the inhibitor taranabant at 2.6 A

123 does not act through the cannabinoid type 1 (CB1) receptor but has many other receptor targets that m

124 rawal in PCP-treated rats via stimulation of CB1 receptors, but reduced social interaction in control

125 ) demonstrate that activation of presynaptic CB1 receptors by retrograde endocannabinoid signaling st

126 aminophen involves an indirect activation of CB1 receptors by the acetaminophen metabolite and endoca

127 Antagonists of the CB1 receptor can be useful in the treatment of several i

128 tments with little but functionally relevant CB1 receptors can be overlooked, fostering an incomplete

129 oid receptors, predominantly the cannabinoid CB1 receptor (CB1 R) in the cerebellum; activation of th

130 We identified an isoform of the human CB1 receptor (CB1b) that is highly expressed in beta-cel

131 imidamides were synthesized and evaluated in CB1 receptor (CB1R) binding assays and iNOS activity ass

132 eceptor interacting protein 1a (CRIP1a) is a CB1 receptor (CB1R) distal C-terminal-associated protein

133 th increased activity of the endocannabinoid/CB1 receptor (CB1R) system that promotes the hepatic exp

134 denosine A2A receptor (A2AR) and cannabinoid CB1 receptor (CB1R), are of pivotal importance in the co

135 du(2J) mutation ablated cannabinoid CB1 receptor (CB1R)-mediated modulation of spontaneous n

136 Cannabinoid CB1 receptors (CB1R) are widely distributed in the brain

137 Activation of cannabinoid CB1 receptors (CB1R) by delta9-tetrahydrocannabinol (THC

138 Thus, whereas CB1 receptors (CB1R) uniformly depress excitatory pathwa

139 Cannabinoid CB1 receptors (CB1Rs) mediate the presynaptic effects of

140 to be mediated by activation of cannabinoid CB1 receptors (CB1Rs) on GABAergic neurons that disinhib

141 minergic D2 receptors (D2Rs) and cannabinoid CB1 receptors (CB1Rs), both critical for LTD induction i

142 emerged as excellent tools for investigating CB1 receptors' cell-type-specific localization and suffi

143 Brain cannabinoid CB1 receptors contribute to alcohol-related behaviors in

144 Presynaptic CB1 receptors control midbrain dopamine neuron activity

145 -2 induction by Delta(9)-THC is mediated via CB1 receptor-coupled G protein betagamma subunits.

146 The molecular basis of CB1 receptor coupling to its cognate G protein is unknow

147 In vitro, primary cultures of CB1 receptor-deficient KC released increased amounts of

148 In vivo, contact allergic ear tissue of CB1 receptor-deficient KCs showed enhanced expression of

149 gonists as well as data from tissue-specific CB1 receptor-deficient mice suggest the rostral ventrome

150 CB1 receptor-deficient mice were previously shown to hav

151 , we partly restored the phenotype of global CB1 receptor deletion in anxiety-like behaviors and full

152 e CB1 receptor gene (CNR1) that may moderate CB1 receptor density.

153 n-induced suppression of excitation (DSE), a CB1 receptor-dependent form of synaptic plasticity at gl

154 1 receptor signaling was down-regulated, and CB1 receptor-dependent long-term depression at DLS synap

155 a temporal behavioral response pattern in a CB1 receptor-dependent manner--suggesting that cannabino

156 ented the aversive effects of acute MWD by a CB1 receptor-dependent mechanism.

157 ipase (MAGL) that hydrolyzes 2-AG, induced a CB1 receptor-dependent reduction of the frequency of mEP

158 whether the effects of the stimulation were CB1 receptor-dependent.

159 Mice with a KC-specific deletion of CB1 receptors developed increased and prolonged CHS resp

160 CB1 -RS and GABA-CB1 -RS mice show the usual CB1 receptor distribution and expression in hippocampal

161 synapses of VTA DA neurons primarily due to CB1 receptor downregulation.

162 dicate that anandamide-mediated signaling at CB1 receptors, driven by oxytocin, controls social rewar

163 macological manipulations in mice expressing CB1 receptors exclusively in DBH(+) cells revealed that

164 promotes an intermediate conformation of the CB1 receptor, explaining ORG27569's ability to increase

165 l knock-out mice revealed necessary roles of CB1 receptor expressed in dorsal telencephalic glutamate

166 hether these rescue mice maintain endogenous CB1 receptor expression level, detailed anatomical studi

167 d as an alternative approach to modulate the CB1 receptor for therapeutic benefits.

168 peutics aimed at blocking the cannabinoid 1 (CB1) receptor for treatment of obesity resulted in signi

169 The absence of CB1 receptors from GABAergic neurons led to a depression

170 nd AM 404 to hoxB8-CB1(-/-) mice, which lack CB1 receptors from the peripheral nervous system and the

171 Deletion of cannabinoid type 1 (CB1) receptors from cortical projections originating in

172 4 Hz stimulation reduces Cb1 receptor function by (i) increasing the rate of endo

173 Ms) offer an alternative approach to enhance CB1 receptor function for therapeutic gain with the prom

174 aired eCB-LTD revealed that PE downregulated CB1 receptor function.

175 etic strategy to reconstitute full wild-type CB1 receptor functions exclusively in dorsal telencephal

176 mmon functional variation (rs2023239) in the CB1 receptor gene (CNR1) that may moderate CB1 receptor

177 posure were reminiscent of those elicited by CB1 receptor genetic ablation, and CB1-null mice were re

178 gical or genetic invalidation of cannabinoid CB1 receptors has been linked to depression in humans an

179 Allosteric modulators of the cannabinoid CB1 receptor have recently been reported as an alternati

180 ockin mice with cell-type-specific rescue of CB1 receptors have emerged as excellent tools for invest

181 nophen, and the precise site of the relevant CB1 receptors have remained elusive.

182 oids and their attending cannabinoid type 1 (CB1) receptor have been implicated in animal models of p

183 nce or unwanted side effects associated with CB1 receptors; however, the signaling profile of AM1710

184 mpal CA1 stratum radiatum, the values of the CB1 receptor-immunopositive excitatory and inhibitory sy

185 The proportion of CB1 receptor-immunopositive excitatory and inhibitory sy

186 ely reported neuroprotective activity of the CB1 receptor in animal models, the precise pathophysiolo

187 These data reveal that CB1 receptor in dorsal telencephalic glutamatergic neuro

188 Deletion of CB1 receptor in GABAergic neurons in GABA-CB1-KO mice le

189 In contrast, in mice lacking CB1 receptor in glutamatergic cells (Glu-CB1-KO), hippoc

190 multiple sclerosis; conditional deletion of CB1 receptor in peripheral nerves; side-effect profiling

191 of alcohol abuse suggests an involvement of CB1 receptors in alcohol dependence in humans.

192 We measured CB1 receptors in alcohol dependent patients in early and

193 ty of [(18)F]FMPEP-d 2, and then to quantify CB1 receptors in alcoholic patients (n = 18) and chronic

194 a widespread approximately 20% reduction of CB1 receptors in alcoholic subjects, without significant

195 ncourage the study of cannabinoids acting on CB1 receptors in chronic gastrointestinal disorders, esp

196 rexigenic mediators that act via cannabinoid CB1 receptors in hypothalamus, limbic forebrain, and bra

197 Genetic deletion and rescue of CB1 receptors in specific cell types revealed that the C

198 that act as inverse agonists of cannabinoid CB1 receptors in the brain can attenuate the rewarding a

199 iated by two types of cannabinoid receptors, CB1 receptors in the nervous system and CB2 receptors in

200 opic effects, it has been suggested that the CB1 receptors in the periphery could play a significant

201 nvestigated the requirement for signaling at CB1 receptors in the reconsolidation of a previously con

202 y the functional interaction between MOP and CB1 receptors in vivo.

203 ain central molecular target, cannabinoid-1 (CB1) receptors in man.

204 nt discovery of allosteric modulators of the CB1 receptor including PSNCBAM-1 (4) has generated signi

205 acellular loops 2 and 3 (IC2 and IC3) of the CB1 receptor, including Ile-218(3.54), Tyr-224(IC2), Asp

206 essary and sufficient for down-regulation of Cb1 receptors induced by 4 Hz stimulation.

207 y and amplitude of mEPSCs in the presence of CB1 receptor inhibition.

208 eurexin knockout phenotype was attenuated by CB1-receptor inhibition, which blocks presynaptic endoca

209 Here, we identify the mediators of CB1 receptor internalization and ORG27569-induced G prot

210 show the critical role of beta-arrestin 2 in CB1 receptor internalization upon treatment with CP55940

211 and reinstatement in squirrel monkeys by the CB1-receptor inverse agonist rimonabant and by the recen

212 thereby emulating the effect of cannabinoid CB1-receptor inverse agonists.

213 The cannabinoid CB1 receptor is expressed in different neuronal subpopul

214 The cannabinoid CB1 receptor is involved in complex physiological functi

215 Consequently, if the CB1 receptor is lost in either neuronal population, an a

216 The cannabinoid (CB1) receptor is a member of the rhodopsin-like G protei

217 In the hippocampus, cannabinoid type 1 (CB1) receptor is present on both GABAergic and glutamate

218 ctivation of presynaptic cannabinoid type-1 (Cb1) receptors is reduced at parallel fibre synapses in

219 the potential relevance to diabetes of human CB1 receptor isoforms in extraneural tissues involved in

220 tion rate constant for [(3)H]-CP55940 at the CB1 receptor, (kfast without: 1.2 +/- 0.2/min; with: 3.8

221 Results were compared with conditional CB1 receptor knockout lines.

222 Global and conditional CB1 receptor-knockout mice were used as controls.

223 Endocannabinoid activation of cannabinoid (CB1) receptors known to inhibit presynaptic GABA release

224 ent with reported effects in tissue-specific CB1 receptor KO mice, we conclude that the metabolic ben

225 both capsaicin and the endogenous TRPV1 and CB1 receptor ligand anandamide (ACR neurons).

226 ocally identify the restricted population of CB1 receptors located on glutamatergic terminals as an i

227 By pharmacologically targeting the CB1 receptors, marijuana has preferential access to this

228 These results suggest that abnormal CB1 receptor-mediated anandamide signaling is implicated

229 d place preference or aversion, but elicited CB1 receptor-mediated antinociceptive effects in the chr

230 As a first step toward understanding CB1 receptor-mediated G protein signaling, we have const

231 Chronic restraint stress also reduced the CB1 receptor-mediated inhibition of EPSC and the eCB-med

232 hile considerable evidence demonstrates that CB1 receptor-mediated modulation of emotional processing

233 An endocannabinoid CB1 receptor-mediated suppression of GABA(B) receptor ac

234 AM1710 (10 mg/kg, i.p.) did not precipitate CB1 receptor-mediated withdrawal in mice rendered tolera

235 We show that cannabinoid CB1-receptor-mediated short-term synaptic plasticity in

236 The cannabinoid type 1 (CB1) receptor mediates marijuana's psychoactive and rein

237 Thus, CB1 receptors modulate bidirectional circuits between th

238 y also regulating synaptic input to the NAc, CB1 receptors modulate NAc output onto downstream neuron

239 her demonstrate that this same population of CB1 receptors modulates optical self-stimulation sustain

240 -induced suppression of inhibition (DSI) and CB1 receptor modulation only at IT cells.

241 ist rimonabant and by the recently developed CB1-receptor neutral antagonist AM4113.

242 These findings point to CB1-receptor neutral antagonists as a new class of medic

243 The recently developed CB1-receptor neutral antagonists may provide an alternat

244 recordings in murine slice preparations from CB1 receptor-null mice and green fluorescent protein hem

245 g GABAergic interneurons possessed increased CB1 receptor number, active-zone complexity and receptor

246 the possibility of a negative regulation by CB1 receptors of leptin-mediated ROS formation in the AR

247 The subcellular distribution of hippocampal CB1 receptors of rescue mice that express the gene exclu

248 By comparison, the rescue of the CB1 receptor on dorsal telencephalic glutamatergic neuro

249 uences of cell-type-specific deletion of the CB1 receptor on the induction of hippocampal LTP and on

250 Thus, CB1 receptors on adrenergic and noradrenergic cells prov

251 This modulation requires CB1 receptors on cortical glutamatergic afferents.

252 ach to identify the relative contribution of CB1 receptors on epidermal KCs for the control of CHS re

253 inoids that activate presynaptic cannabinoid CB1 receptors on juxtaposing axon terminals.

254 is depends on intact cannabinoid receptor 1 (CB1) receptors on forebrain GABAergic neurons and pain r

255 Blocking or deleting the CB1 receptor only reduces both anandamide- and capsaicin

256 stration of a CB2-preferring agonist engages CB1 receptors or produces CB1-mediated side effects is u

257 Given the side effects associated with CB1 receptor orthosteric antagonists, negative allosteri

258 AGL contribute to 2-AG clearance and prevent CB1 receptor over-stimulation in the cerebellum.

259 ontractions in isolated guinea pig ileum via CB1 receptors (pEC50, 6.0 +/- 0.4).

260 se pathophysiological relevance of those two CB1 receptor pools in neurodegenerative processes is unk

261 ors in specific cell types revealed that the CB1 receptor population specifically in dopamine beta-hy

262 uced impairment of memory consolidation, but CB1 receptors present in other neuronal populations are

263 Moreover, blockade of BNST CB1 receptors prevented increases in time-out responding

264 n CFA-treated rats correlated with decreased CB1 receptor protein expression and function in the RVM.

265 d a PBIF for [(18)F]FMPEP-d 2, a cannabinoid CB1 receptor radioligand, in healthy volunteers, and als

266 sed on improving potency and efficacy at the CB1 receptor, reducing lipophilicity and limiting the ce

267 n leads to downregulation of the cannabinoid CB1 receptor (referred to as CB1 in the Cutando et al. a

268 Given CB1 receptors remain as potential pharmacological target

269 The CB1 receptor represents a promising target for the treat

270 ammatory pain, and suggest that the relevant CB1 receptors reside in the rostral ventromedial medulla

271 , specific and exclusive deletion of hepatic CB1 receptor resulted in a rescue of the dyslipidemic ef

272 4-chlorophenyl position for activity at the CB1 receptor, resulting in several analogs with comparab

273 for either PPAR-alpha (MK886) or cannabinoid CB1 receptors (rimonabant).

274 nocking out CB1 receptors, and (ii) deleting CB1 receptors selectively in corticostriatal glutamaterg

275 c acid to conditional mutant animals lacking CB1 receptors selectively in GABAergic or glutamatergic

276 of 0.5 nM) and the best selectivity over the CB1 receptor (selectivity index of 2594).

277 Disturbances in cortical cannabinoid CB1 receptor signaling are well established correlates o

278 Fasting/refeeding experiments revealed that CB1 receptor signaling in many specific brain neurons is

279 Together, these results indicate that the CB1 receptor signaling system both on inhibitory and exc

280 Following CIE, DLS endocannabinoid CB1 receptor signaling was down-regulated, and CB1 recep

281 Positive allosteric modulation of CB1-receptor signaling shows promise as a safe and effec

282 ors, we demonstrated that ORG27569 induces a CB1 receptor state that is characterized by enhanced ago

283 tute a critical period during which repeated CB1 receptor stimulation is sufficient to elicit an endu

284 Furthermore, CB1 receptor substrates functionally interact with opiat

285 s, whereas activation of the endocannabinoid CB1 receptor suppresses these responses.

286 Activation of cannabinoid CB1 receptors suppresses pathological pain but also prod

287 a potent, orally absorbed antagonist of the CB1 receptor that is >50-fold selective for CB1 over CB2

288 as a proinflammatory chemokine regulated by CB1 receptors that promotes immune cell recruitment to a

289 ut it enhanced affinity of anandamide at the CB1 receptor, thereby potentiating the effects of this e

290 However, the role of mPFC CB1 receptor transmission in the modulation of behaviora

291 Modulation of cannabinoid CB1 receptor transmission within the medial prefrontal c

292 sues are abolished by the lack of functional CB1 receptor via direct peripheral effect and partially

293 The role of the CB1 receptor was explored using CB1-knockdown (CB1Kd) in

294 Baseline availability of the CB1 receptor was studied using PET with [(11)C]MePPEP, a

295 Indeed, acute pharmacological blockade of CB1 receptors was sufficient to rescue the altered remot

296 o understand the unexpected affinity for the CB1 receptor, we devised a 3D-QSAR model, which we then

297 Allosteric modulators of the cannabinoid CB1 receptor were first discovered in 2005.

298 The human CB1 receptor, which is among the most expressed receptor

299 ion of IPSCs was mediated by the cannabinoid CB1 receptors, while DHPG-induced I-LTD was dependent on

300 he agonist-induced G-protein coupling to the CB1 receptor, yet induced beta-arrestin mediated ERK1/2