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1 es have evaluated the therapeutic effects of cannabinoids.
2 e snapshots of the molecular pharmacology of cannabinoids.
3 is chemotypes divergent for alkyl and cyclic cannabinoids.
4 erpenoids, monoterpene indole alkaloids, and cannabinoids.
5 rstand how basal ganglia (BG) is affected by cannabinoids.
6 al disorders might therefore be treated with cannabinoids.
10 olescence resulted in the down-regulation of cannabinoid 1 receptors (CB(1)Rs) in adulthood in a sex
12 mote energy conservation in obesity, whereas cannabinoid-1 receptor (CB(1) R) blockade reverses body
16 ncipal biosynthetic enzyme of the endogenous cannabinoid 2-arachidonylglycerol (2-AG) on neurons, pla
18 ndances of nearly all of the dozens of known cannabinoids(4), and their structural complexity, which
20 soprenylated resorcinyl polyketides known as cannabinoids, a subset of which are medically important
23 this study, we evaluated whether (synthetic) cannabinoid activity can be detected in oral fluid (OF)
24 compounds, makes understanding how exogenous cannabinoids affect brain development an important biome
26 f the nutraceutically important amino acids, cannabinoids, alkaloids, and fatty acids, the high altit
28 terminants underlying in planta variation of cannabinoid alkyl side-chain length remain uncharacteris
31 atty acids to our engineered strains yielded cannabinoid analogues with modifications in the part of
33 tion to raising concerns about the safety of cannabinoid and alcohol exposure during early embryonic
34 ) in complex with an "ultrapotent" synthetic cannabinoid and its G protein (Krishna Kumar et al., 201
35 as an unprecedented mechanistic link between cannabinoids and motor performance, and suggest that act
36 onstrates that mice voluntarily consume both cannabinoids and opioids via gelatin, and that cannabino
39 f genes involved in the biosynthesis of both cannabinoids and terpenoids from imported precursors.
43 acterize the plasma pharmacokinetics (PK) of cannabinoids and their metabolites in cattle after a sin
44 luding medicinal cannabis and pharmaceutical cannabinoids and their synthetic derivatives, such as te
45 vercome pharmacokinetic challenges with oral cannabinoids, and to uncover the exact mechanisms by whi
48 al studies show that 'medicinal' cannabis or cannabinoid-based medications relieve pain in human dise
49 ough progress has been made in understanding cannabinoid binding and receptor activation, detailed kn
50 hemp variety "Finola." The map reveals that cannabinoid biosynthesis genes are generally unlinked bu
52 oelectron microscopy structures of synthetic cannabinoid-bound CB2 and CB1 in complex with G(i), as w
53 bolism) counteracts the rewarding effects of cannabinoids by acting as a negative allosteric modulato
56 neurobiological evidence demonstrating that cannabinoids can also alter the brain's initial molecula
57 eport the complete biosynthesis of the major cannabinoids cannabigerolic acid, Delta(9)-tetrahydrocan
60 gy-modulating strategies in vivo showed that cannabinoid CB(1) receptors located on neurons belonging
65 f endocannabinoids that activate presynaptic cannabinoid CB1 receptors on juxtaposing axon terminals.
70 ong to the phenylethylamine, tryptamine, and cannabinoid chemical classes for treating mental health
72 er previously identified peripherally active cannabinoid compounds, and could have clinical applicati
76 species (C. indica and C. sativa), and major cannabinoid contents (tetrahydrocannabinol, THC; and can
79 Under on-chip exposure to the psychoactive cannabinoid, Delta-9-tetrahydrocannabinol (THC), cerebra
80 2-AG or AEA activate NPR-19 directly and cannabinoid-dependent inhibition can be rescued in npr-1
82 ependent signaling pathway that involves the cannabinoid-dependent release of both serotonin and dopa
84 buspirone does not improve outcomes and that cannabinoids do not increase abstinence rates (moderate
85 Delta(9)-tetrahydrocannabinol or a synthetic cannabinoid during the first 10 days of postnatal develo
87 ther, pharmacologically enhancing endogenous cannabinoids (eCB) with JZL184 prevents abstinence-induc
88 ns further reveal that cholesterol regulates cannabinoid enhancement of GlyR function through both di
90 ndrome have had recent exposure to synthetic cannabinoids, evidence of isolated vitamin K antagonism
94 misregulation in animal models of perinatal cannabinoid exposure (using synthetic cannabinoids or ac
95 preclinical data demonstrate that adolescent cannabinoid exposure reprograms the initial behavioral,
99 rise evidence regarding the effectiveness of cannabinoids for medicinal use and describe approaches t
100 ing interest in the therapeutic potential of cannabinoids for neurological disorders such as epilepsy
102 t evidence to provide guidance on the use of cannabinoids for treating mental disorders within a regu
107 alysis, and that the interpretative value of cannabinoid hair measurements from people reporting appl
108 f pain, but long-term treatment of pain with cannabinoids has been challenging to implement in precli
110 However, the study and medicinal use of cannabinoids has been hampered by the legal scheduling o
114 inhaled cannabis were more likely to be for cannabinoid hyperemesis syndrome (18.0% vs. 8.4%), and v
117 There is scarce evidence to suggest that cannabinoids improve depressive disorders and symptoms,
118 ning any type and formulation of a medicinal cannabinoid in adults (>=18 years) for treating depressi
120 ural findings from experimental studies with cannabinoids in animals, and studies of hippocampal macr
122 t of Delta(9)-tetrahydrocannabinol and other cannabinoids in food and feed derived from hemp and in f
125 However, intestinal lymphatic transport of cannabinoids in immunocompromised patients requires caut
129 iveness and safety of all types of medicinal cannabinoids in treating symptoms of various mental diso
133 (FUB), a recently emerged illicit synthetic cannabinoid infused in street drugs that have been assoc
134 eed for further detailed characterisation of cannabinoid inheritance to facilitate metabolic engineer
135 uces aversive effects that might explain why cannabinoid is not rewarding in rodents and might also a
137 rticle will provide information on synthetic cannabinoids, LAARs, and coagulopathic manifestations ar
142 em, not only because it is able to recognize cannabinoid ligands but also because of its expression a
143 L-alpha-lysophosphatidylinositol and various cannabinoid ligands, may regulate endocrine function and
146 geted analysis was performed on three common cannabinoids, namely, Delta9-tetrahydrocannabinol, canna
148 s a paucity of information on the effects of cannabinoids on immunity and on outcomes of infection an
149 ity studies directly examining the effect of cannabinoids on treating mental disorders are needed.
151 athy caused by brodifacoum-tainted synthetic cannabinoids or "fake weed" highlight the public health
152 inatal cannabinoid exposure (using synthetic cannabinoids or active components of the cannabis plant)
153 ypically used forced injections of synthetic cannabinoids or isolated cannabis constituents that may
154 eria included "glaucoma" AND "marijuana" or "cannabinoid" or "CBD." The top 20 Google search and YouT
155 Monoterpenes, sesquiterpenes, hydrocarbons, cannabinoids, other terpenoids, and fatty acids were con
159 cholesterol reduction significantly inhibits cannabinoid potentiation of glycine-activated currents i
161 The system provides an efficient route to cannabinoid precursors cannabigerolic acid (CBGA) and ca
165 nnabinoids and opioids via gelatin, and that cannabinoids provide long-term relief of chronic pain st
168 itionally, we found that capsaicin increased cannabinoid receptor (CB2) in the cochlea, which leads t
172 are expressed in the MHb and MSDB, and that cannabinoid receptor 1 (CB1) is expressed in the MSDB.
174 -enhancing and analgesic effects through the cannabinoid receptor 1 (CB1), a G protein-coupled recept
176 augmentation of AEA signaling and via direct cannabinoid receptor 1 stimulation with Delta(9)-tetrahy
177 As both neurons and glial cells express cannabinoid receptor 1, genetic vulnerability could infl
179 xy-benzo(c) chromen-6-one), a cannabilactone cannabinoid receptor 2 (CB2) agonist, suppresses chemoth
180 rachidonoylglycerol (2-AG) and its receptor, cannabinoid receptor 2 (CB2), play a role in the establi
181 ol (2-AG), and elucidated a hitherto unknown cannabinoid receptor 2 (CB2)-mediated regulatory role of
182 t time, that transient administration of the cannabinoid receptor 2 antagonist AM630 (10 mg/kg) or in
184 abinoid reporter system, which monitored the cannabinoid receptor activation, was compared to the qua
185 In Caenorhabditis elegans, the endogenous cannabinoid receptor agonist, 2-arachidonoylglycerol (2-
186 The rapid proliferation of new synthetic cannabinoid receptor agonists (SCRAs) has initiated cons
189 ed the effects and mechanism(s) of action of cannabinoid receptor agonists, including Delta9-THC, on
190 eport that solubilization of a GPCR, type II cannabinoid receptor CB(2), in a Facade detergent enable
194 t, upon simultaneous ex-pression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same sig
195 he present study demonstrates that mammalian cannabinoid receptor ligands activate a conserved cannab
197 itor tacrine and a benzimidazole-based human cannabinoid receptor subtype 2 (hCB(2)R) agonist and inv
199 - or heterooligomerization between the GPCRs cannabinoid receptor type 1 (CB(1)R) and 5-hydroxytrypta
200 9-THC in endotoxemic mice were reversed by a cannabinoid receptor type 1 (CB(1)R) inverse agonist (SR
201 duced neuronal maturation, downregulation of cannabinoid receptor type 1 (CB1) receptors, and impaire
203 preclinical models, peripherally restricted cannabinoid receptor type 1 (CB1R) inhibitors, which are
204 ness of purposeful movements was reverted by cannabinoid receptor type 1 (CB1r) manipulations directl
206 ent report, we aimed to further evaluate the cannabinoid receptor type 1 (CB1R)-mediated mechanisms i
207 her putative Delta9-THC receptors, including cannabinoid receptor type 2, TRPV1, GPR18, GPR55, and GP
208 lucose-feedback sensor) and CNR2 (encoding a cannabinoid receptor) as central effectors of B-lymphoid
209 tein-coupled receptor (GPR) 55 is a putative cannabinoid receptor, and l-alpha-lysophosphatidylinosit
210 19-null animals by the expression of a human cannabinoid receptor, CB1, highlighting the orthology of
211 s a transient window when the dominant brain cannabinoid receptor, CB1R, is expressed on afferent ter
213 e endocannabinoids and their target, the CB1 cannabinoid receptor, in the adaptation of the brain to
214 ing the allosteric binding site on the CB(1) cannabinoid receptor, in which a CF(3) group successfull
215 oid signaling system mediated by a canonical cannabinoid receptor, NPR-19, with orthology to human CB
218 Here, we investigated structural changes in cannabinoid-receptor 1 (CB(1))-mediated long-term depres
221 n the brain, endocannabinoids act via Type 1-cannabinoid receptors (CB1) to modulate synaptic transmi
223 te the effects of blocking TRPV1 or specific cannabinoid receptors 1 (CB1r) and 2 (CB2r) on periodont
226 ugh it shares low sequence homology with the cannabinoid receptors CB(1)R and CB(2)R, a growing body
229 ral precision of signaling at neuronal CB(1) cannabinoid receptors, chiefly deregulating Stat3-depend
230 A-derived endocannabinoids desensitize CB(1) cannabinoid receptors, thus inducing epigenetic repressi
239 confirmed by behavioral experiments in which cannabinoid-related slowness of purposeful movements was
240 on between both methods, indicating that the cannabinoid reporter assay can be used for an estimation
245 AS and CBDAS genotypes were scored and alkyl cannabinoid segregation analysed in 210 F(2) progeny der
249 odents exposed to repeated administration of cannabinoids show persistent microstructural changes in
251 atterns for expression of genes relevant for cannabinoid signaling (from Allen Human Brain Atlas post
252 tractable, mammalian predictive model, where cannabinoid signaling at the molecular/neuronal levels c
253 etically tractable, whole-animal model where cannabinoid signaling at the molecular/neuronal levels c
254 /ion channels whose overall contributions to cannabinoid signaling have yet to be fully assessed.
255 focused on assessing CB(1)/CB(2)-independent cannabinoid signaling in a genetically tractable, whole-
256 g both CB(1)/CB(2)-dependent and independent cannabinoid signaling pathways in a genetically tractabl
257 binoid receptor ligands activate a conserved cannabinoid signaling system in C. elegans and also modu
259 (PPARs) have been identified as part of the cannabinoid signaling system: both phytocannabinoids and
260 tially physiologically restricted endogenous cannabinoid signaling, may be more vulnerable to the eff
261 the complexities of CB(1)/CB(2)-independent cannabinoid signaling, the role of TRP channels in the m
265 hemotypically extreme pools revealed a known cannabinoid synthesis pathway locus as well as a series
266 NPSs including synthetic opioids, synthetic cannabinoids, synthetic cathinones, and piperazines in t
267 0 NPS residues (synthetic opioids, synthetic cannabinoids, synthetic cathinones, piperazines, indole,
268 ignals.SIGNIFICANCE STATEMENT The endogenous cannabinoid system plays diverse roles in brain developm
269 cts mapped onto biomarkers of the endogenous cannabinoid system providing insight into possible mecha
273 These results highlighted the importance of cannabinoids testing of food products in view of the cur
274 for the production of natural and unnatural cannabinoids that will allow for more rigorous study of
276 by mothers during lactation transfers active cannabinoids to the developing offspring during this cri
277 gs, drugs for neuropathic pain, opioids, and cannabinoids, to physical therapy strategies and prevent
279 that cocaine-memory reconsolidation requires cannabinoid type 1 receptor (CB1R) signaling based on th
281 e pre-phase of arthritis using butyrate or a cannabinoid type 1 receptor agonist inhibits the develop
282 and a selectivity factor of nearly 700 over cannabinoid type 1 receptors, target compound 3 exhibite
287 ndocannabinoid system, and in particular the cannabinoid type 2 receptor (CB2R), raised the interest
289 aptic responses by activation of presynaptic cannabinoid type-1 (Cb1) receptors is reduced at paralle
290 reviously reported diarylurea derivatives as cannabinoid type-1 receptor (CB(1)) allosteric modulator
291 2R and moderate to good selectivity over the cannabinoid type-1 receptor (CB1R), associated with good
292 ng in male rats via glucocorticoid-dependent cannabinoid type-1 receptor (CB1R)-mediated actions in t
294 late the signal transduction pathways of the cannabinoid type-2 receptor (CB2R) can represent a helpf
296 creasing evidence suggests that psychoactive cannabinoid use in adolescence enhances the behavioral e
297 try method for the quantification of fifteen cannabinoids was developed and validated for multiple ma
298 nthocyanidins, phytic acid, lignanamides and cannabinoids were determined from the separated phases.
299 are involved in the tetrad assay induced by cannabinoids which had been associated with CB1R agonism