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1 ed increased responses to elevated levels of endogenous cannabinoids.
2 and immunological actions of Delta(9)THC and endogenous cannabinoids.
3 ating the cognitive actions of marijuana and endogenous cannabinoids.
4 t it is mediated by the autocrine release of endogenous cannabinoids.
5 smission that involves the production of the endogenous cannabinoid 2-arachidonoyl glycerol (2-AG).
6 rrelation between enhanced production of the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) and
7 ility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in
9 embrane serine hydrolase that hydrolyzes the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) to
10 iatal levels of AEA, but not the other major endogenous cannabinoid 2-arachidonoylglycerol (2-AG), du
11 e demonstrate that rat platelets contain the endogenous cannabinoid 2-arachidonyl glyceride (2-AG), a
14 ting fatty acid amides including anandamide (endogenous cannabinoid agonist) and oleamide (sleep-indu
15 nsible for the degradation of anandamide, an endogenous cannabinoid agonist, and oleamide, a sleep-in
16 ylglycerol (2-AG) are the most characterized endogenous cannabinoids (also known as endocannabinoids)
19 omodulatory fatty acid amides, including the endogenous cannabinoid anandamide and the sleep-inducing
20 omodulatory fatty acid amides, including the endogenous cannabinoid anandamide and the sleep-inducing
21 omodulatory fatty acid amides, including the endogenous cannabinoid anandamide and the sleep-inducing
22 yme that degrades lipid amides including the endogenous cannabinoid anandamide and the sleep-inducing
23 lass of lipid transmitters that includes the endogenous cannabinoid anandamide and the sleep-inducing
24 ogenous signaling lipids, which includes the endogenous cannabinoid anandamide and the sleep-inducing
25 or the uptake and cellular processing of the endogenous cannabinoid anandamide are not well understoo
26 cilitated transport process that removes the endogenous cannabinoid anandamide from extracellular spa
28 permitted measurement of the release of the endogenous cannabinoid anandamide in the periaqueductal
30 to the synthetic cannabinoid HU-210 and the endogenous cannabinoid anandamide led to significant ind
33 cluding known signaling molecules (e.g., the endogenous cannabinoid anandamide) and a novel family of
38 binoid receptors, CB1 and CB2, and the major endogenous cannabinoids (anandamide and 2-arachidonoyl g
39 id effect was mimicked by application of the endogenous cannabinoid, anandamide and blocked by VR1 an
42 achidonoylglycerol (2-AG), the most abundant endogenous cannabinoid and a full agonist for cannabinoi
44 ing cannabinoid receptors using exogenous or endogenous cannabinoids and use of FAAH inhibitors may c
45 platelets and macrophages generate different endogenous cannabinoids, and that both 2-AG and anandami
46 is thought that the physiological actions of endogenous cannabinoid arachidonylethanolamide (AEA), as
47 porting a possible physiological role for an endogenous cannabinoid, arachidonylethanolamide (AEA, an
50 endocrine output, presaging the emergence of endogenous cannabinoids as important signalling molecule
51 stem consisting of cannabinoid receptors and endogenous cannabinoids as well as the enzymatic machine
53 to develop drugs that amplify the effects of endogenous cannabinoids by preventing their inactivation
55 In contrast to classical neurotransmitters, endogenous cannabinoids can function as retrograde synap
57 regnancy has the potential to interfere with endogenous cannabinoid (CB) regulation of fetal nervous
58 en reported to be activated by exogenous and endogenous cannabinoid compounds but surprisingly also b
61 correlates that accompany the disruption of endogenous cannabinoid (eCB) signaling in a food-motivat
64 presents a primary degradation enzyme of the endogenous cannabinoid (eCB), 2-arachidonoyglycerol (2-A
65 t GABAergic inhibition in DGCs is subject to endogenous cannabinoid (eCB)-mediated retrograde regulat
67 e current study to investigate if intraislet endogenous cannabinoids (ECs) regulate beta-cell prolife
69 acid amide hydrolase (FAAH) inactivates the endogenous cannabinoid (endocannabinoid) anandamide and
74 ly inhibited by cannabinoids in the NAc, and endogenous cannabinoids (endocannabinoids) play a critic
75 m potentiation (LTP) in the hippocampus, yet endogenous cannabinoids (endocannabinoids) transiently s
76 The ECS comprises cannabinoid receptors, endogenous cannabinoids (endocannabinoids), and the enzy
77 omprising CB1 and CB2 cannabinoid receptors, endogenous cannabinoids (endocannabinoids), and the enzy
79 t in vitro studies have described a role for endogenous cannabinoids ("endocannabinoids") as transsyn
84 (2-AG) and depolarization-induced release of endogenous cannabinoids have minimal effect on mIPSC fre
85 findings suggest that Purkinje cells release endogenous cannabinoids in response to elevated calcium,
86 these findings suggest a widespread role for endogenous cannabinoids in retrograde synaptic inhibitio
89 l cells were treated with both synthetic and endogenous cannabinoids in vitro, and biochemical coupli
91 se findings strongly suggest that release of endogenous cannabinoids is involved in brain reward proc
92 nt, retrograde inhibition of GABA release by endogenous cannabinoids is persistently enhanced in the
95 Our results indicate that 2-AG is a second endogenous cannabinoid ligand in the central nervous sys
99 of anandamide (arachidonylethanolamide), an endogenous cannabinoid lipid, are terminated by a two-st
100 The effect of SR 141716A suggests that an endogenous cannabinoid may mediate striato-nigral transm
101 vel of the thalamus and that one function of endogenous cannabinoids may be to modulate pain sensitiv
102 y CB1 cannabinoid receptors, indicating that endogenous cannabinoids may contribute to the control of
104 141716A was used to test the hypothesis that endogenous cannabinoids modulate tonic pain sensitivity.
105 plays a central role in the lifecycle of the endogenous cannabinoid N-arachidonoylethanolamine (anand
106 deducing the bioactive conformation of these endogenous cannabinoids, not only at the CB receptors bu
107 rform a comparative study with synthetic and endogenous cannabinoids on their effects on synaptic con
109 These findings suggest that exogenous and endogenous cannabinoids potentiate GlyRs via a hydrogen
113 and this molecule is well established as an endogenous cannabinoid receptor agonist in the brain.
114 The present study demonstrates that the endogenous cannabinoid receptor agonists 2-arachidonoylg
121 ction of THC is specific (i.e., mediated via endogenous cannabinoid receptors) or non-specific, refle
122 lation of appetite hormones mediated through endogenous cannabinoid receptors, independent of glucose
124 ting that retrograde synaptic suppression by endogenous cannabinoids represents a widespread signalin
125 e (FAAH), which leads to increased levels of endogenous cannabinoids, resulted in decreased liver inj
126 rotransmission, raising the possibility that endogenous cannabinoids serve naturally to modulate pain
129 e consistent with a neuroprotective role for endogenous cannabinoid signaling pathways and with a pot
132 olar cells suggest a substantive role for an endogenous cannabinoid signaling system in retinal physi
133 iterature on the effects of cannabinoids and endogenous cannabinoid signaling systems in the regulati
134 nisms of action, including a facilitation of endogenous cannabinoid signaling via one of its metaboli
137 ication and quantification of anandamide, an endogenous cannabinoid substance, and other fatty acid e
138 anandamide (N-arachidonoylethanolamine), an endogenous cannabinoid substance, may be produced throug
141 the release of anandamide, but not of other endogenous cannabinoids such as 2-arachidonylglycerol.
142 ls, but there is only indirect evidence that endogenous cannabinoids such as anandamide participate i
143 The IPSCs are regulated by exogenous and endogenous cannabinoids, suggesting that they arise from
145 link between functional abnormalities in the endogenous cannabinoid system and drug abuse and depende
148 Although emerging evidence implicates the endogenous cannabinoid system in aspects of opioid and e
151 results suggest that neuroadaptations in the endogenous cannabinoid system may be part of the neuropl
152 ing SR141716A and SR144528 indicate that the endogenous cannabinoid system may be tonically active in
155 butable to the disruption by cannabis of the endogenous cannabinoid system's spatiotemporal regulatio
157 wal has been established via discovery of an endogenous cannabinoid system, identification of cannabi
161 n, stress elicits the rapid formation of two endogenous cannabinoids, the lipids 2-arachidonoylglycer
162 mponent found in marijuana or anandamide, an endogenous cannabinoid, to DC cultures induced apoptosis
163 investigation uncovered a specific role for endogenous cannabinoid tone in timing behavior, as eleva
164 of anandamide signaling in vivo, setting an endogenous cannabinoid tone that modulates pain percepti
166 udies have demonstrated that the majority of endogenous cannabinoid type 1 (CB(1)) receptors do not r
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