ライフサイエンスコーパス: CB1 receptor

1 did not display affinity for the cannabinoid CB1 receptor.

2 ylglycerol (2-AG) that activates 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 ve improved affinity and selectivity for the CB1 receptor.

7 ynthesized and assessed for allostery of the CB1 receptor.

8 ry targeting the pharmacologically important CB1 receptor.

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

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

11 semble those observed in animals lacking the CB1 receptor.

12 ptic strengths via presynaptically-expressed CB1 receptors.

13 fects of JZL184 were mediated by cannabinoid CB1 receptors.

14 king, both tightly controlled by cannabinoid CB1 receptors.

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

16 -administration and is tightly controlled by CB1 receptors.

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

18 effects are related to local availability of CB1 receptors.

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

20 through antagonism of peripherally expressed CB1 receptors.

21 c transmission via presynaptically expressed CB1 receptors.

22 7 nM), and moderate to good selectivity over CB1 receptors.

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

24 e similarly modulated by activation of these CB1 receptors.

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

26 by pharmacological or genetic inhibition of CB1 receptors.

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

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

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

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

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

32 CB1 receptor activation in the vlPAG attenuated dural-ev

33 ass unwanted central effects associated with CB1 receptor activation.

34 211 did not produce cardinal signs of direct CB1-receptor activation in the presence or absence of pa

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

36 ocannabinoid levels and hence on cannabinoid CB1 receptor activity.

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

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

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

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

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

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

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

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

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

46 -1 (4) has generated significant interest in CB1 receptor allosteric modulation.

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

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

49 We show that GPR55 and CB1 receptors alter each others signaling properties in

50 0, 7.7 +/- 0.1) and a partial agonist at the CB1 receptor, although with a decrease in functional res

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

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

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

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

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

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

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

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

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

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

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

62 binds selectively to the brain cannabinoid (CB1) receptor and exhibits a potent inverse agonist/anta

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

64 hydrocannabinol, binds to brain cannabinoid (CB1) receptors and activates signal transduction pathway

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

68 sm with SR144528 (1.4 mg kg-1 I.P.).However, CB1 receptor antagonism by rimonabant (4.6mg kg-1 I.P.)

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

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

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

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

79 ous cannabinoids, including analogues of the CB1 receptor antagonist Rimonabant(R), CB2 receptor agon

80 Depression was also blocked by the CB1 receptor antagonist rimonabant, but this is thought

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

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

83 CB1 receptor antagonist-induced hypophagia was fully abo

84 l bilateral microinjection of a cannabinoid (CB1) receptor antagonist (AM251) into PAG.

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

86 Here, we show that CB1 receptor antagonists can act both as agonists alone

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

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

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

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

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

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

93 CB1 receptors are also part of the brain endocannabinoid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 GPR55 and CB1 receptors can form heteromers, but the internalizati

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 and abrogated the sensitivity of cannabinoid CB1 receptors (CB1Rs) controlling GABA synapses in the s

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 ch retrogradely suppresses GABA release from CB1 receptor-containing inhibitory presynaptic boutons.

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

145 Presynaptic CB1 receptors control midbrain dopamine neuron activity

146 -2 induction by Delta(9)-THC is mediated via CB1 receptor-coupled G protein betagamma subunits.

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

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

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

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

151 CB1 receptor-deficient mice were previously shown to hav

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

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

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

155 1 receptor signaling was down-regulated, and CB1 receptor-dependent long-term depression at DLS synap

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

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

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

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

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

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

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

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

164 ogical inhibition or genetic deletion of the CB1 receptor eliminated the pairing-induced long-term sy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 7TM/GPCR and that this interaction with the CB1 receptor has functional consequences in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 e demonstrate that the co-expression of FLAG-CB1 receptors in cells stably expressing HA-GPR55 specif

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

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

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

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

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

202 have indicated that selective regulation of CB1 receptors in the periphery is a viable strategy for

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

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

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

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

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

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

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

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

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

212 Recently, several synthetic CB1 receptor inverse agonists/antagonists, such as SR141

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

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

215 The cannabinoid CB1 receptor is expressed in different neuronal subpopul

216 The cannabinoid CB1 receptor is involved in complex physiological functi

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

218 the current data indicate that activation of CB1 receptors is needed to ameliorate neuropathic SCI pa

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

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

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

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

223 Results were compared with conditional CB1 receptor knockout lines.

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

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

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

227 RG27569-induced conformational change of the CB1 receptor led to cellular internalization and downstr

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

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

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

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

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

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

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

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

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

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

238 Thus, CB1 receptors modulate bidirectional circuits between th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 Given CB1 receptors remain as potential pharmacological target

268 The CB1 receptor represents a promising target for the treat

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

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

271 4-chlorophenyl position for activity at the CB1 receptor, resulting in several analogs with comparab

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

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

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

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

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

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

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

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

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

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

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

283 Furthermore, CB1 receptor substrates functionally interact with opiat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

299 Importantly, a blockade of hippocampal CB1 receptors with AM251 prevented the impairing effect

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