ライフサイエンスコーパス: endogenous opioid

1 receptor (MOP-R) , which is also a target of endogenous opioids.

2 r infant survival and partly mediated by the endogenous opioids.

3 oid autoreceptors that "gate" the release of endogenous opioids.

4 Rs prevent the modulation of this synapse by endogenous opioids.

5 ponses to an immune challenge and a role for endogenous opioids.

6 ting palatability enhanced by the release of endogenous opioids.

7 through CD95-mediated apoptosis dependent on endogenous opioids.

8 editation-based pain relief does not require endogenous opioids.

9 ss-meditation-based analgesia is mediated by endogenous opioids.

10 ed by the separation distress system through endogenous opioids.

11 nia, both of which are strongly modulated by endogenous opioids.

12 siologic effects in vivo compared with other endogenous opioids.

13 rgans, which is likely due to the release of endogenous opioids.

14 amed intestine and expressed a high level of endogenous opioids.

15 e cell plasticity was dependent on action of endogenous opioids.

16 lts suggest receptor-type specific roles for endogenous opioids acting at both pre- and postsynaptic

17 ), corticotropin-releasing factor (CRF), and endogenous opioids acting at mu-opiate receptors.

18 Moreover, endogenous opioids, acting via MOR, within the CeA promo

19 Next, it was determined whether endogenous opioid action mediates sexual reward and memo

20 receptor and the magnitude of stress-induced endogenous opioid activation in these regions accounted

21 clude the anterior cingulate as a center for endogenous opioid activation specific to negative pain a

22 ablishment of maternal memory is mediated by endogenous opioid activity around the time of parturitio

23 years were enrolled in a protocol to measure endogenous opioid activity by inducing opioid receptor b

24 Placebo treatment affected endogenous opioid activity in a number of predicted mu-o

25 Altered endogenous opioid activity in MDD may hinder emotional r

26 opioid peptide-degrading enzymes, stabilizes endogenous opioid agonists released by cAMP-PDE inhibito

27 nduced increase in IL-1beta experienced less endogenous opioid analgesia.

28 These findings indicate altered endogenous opioid analgesic activity in FM and suggest a

29 Endogenous opioid and cannabinoid systems are thought to

30 ion of neurotransmitters responsive to pain (endogenous opioid and dopamine), as well as their regula

31 Endogenous opioid and non-opioid mechanisms (for example

32 suggests that certain stressors release both endogenous opioids and corticotropin-releasing factor (C

33 KEY POINTS: Both endogenous opioids and opiate drugs of abuse modulate le

34 tersection between stress neuromediators and endogenous opioids and so may be a site at which stress

35 ng the well-established interactions between endogenous opioids and stress.

36 brain stem that controls eating and contains endogenous opioids and their receptors.

37 her these reactions are under the control of endogenous opioids and to determine the role of the midb

38 These data together with others suggest that endogenous opioids and/or constitutive activity of MORs

39 Met-enkephalin (mENK), an endogenous opioid, and exogenous opiates such as morphin

40 Endogenous opioids, and in particular mu-opioid receptor

41 num that produce several peptides, including endogenous opioids, and that also express the Trpm5 cati

42 Endogenous opioids are important neuromodulators, and ar

43 Levels of endogenous opioids are increased in morbidly obese human

44 EAE), an animal model of MS, suggesting that endogenous opioids are inhibitory trophic factors in EAE

45 Here we find endogenous opioids are released by synaptic stimulation

46 Furthermore, endogenous opioids, arterial blood pressure and MSNA do

47 tential for biased agonism in the actions of endogenous opioids at the MOP in a common cellular backg

48 regulation of the LC-noradrenergic system by endogenous opioids because of the lack of effect of opia

49 (POMC) neurons as these neurons produce the endogenous opioid beta-endorphin and are heavily regulat

50 oopiomelanocortin (POMC) neurons release the endogenous opioid beta-endorphin and POMC neuron activit

51 amma-melanocyte stimulating hormone; and the endogenous opioid beta-endorphin) have a diverse array o

52 stimulates release from keratinocytes of the endogenous opioid beta-endorphin, which then acts at opi

53 ain typical secretory granules yet expresses endogenous opioids (beta-endorphin and Met-enkephalin) a

54 he stress axis is regulated by, in part, the endogenous opioid, beta-endorphin, acting on mu-opioid r

55 Fear and emotional learning are modulated by endogenous opioids but the cellular basis for this is un

56 pioid receptors is not due to the release of endogenous opioids, but rather to its ligand-independent

57 dministration and to determine if release of endogenous opioids by cocaine is mediated by activation

58 an opportunity for studying the role of this endogenous opioid circuitry, with its regulators, in mod

59 lts suggests differences in the way in which endogenous opioids contribute to the behavioral and neur

60 However, the mechanisms by which endogenous opioids contribute to the pathophysiology of

61 Understanding how endogenous opioids control physiologic processes through

62 compensatory opponent process that generates endogenous opioid dependence.

63 gnaling at opioid receptors, and produces an endogenous opioid-dependent state.

64 not blocked by bicuculline, suggesting that endogenous opioids did not enhance mossy fiber LTP by de

65 ntal performance, the loss of either or both endogenous opioids did not influence preference for wate

66 Although many endogenous opioids displayed signaling profiles similar

67 opioid antagonist naloxone demonstrate that endogenous opioids do not maintain a tonic inhibitory co

68 revious studies show that Met-enkephalin, an endogenous opioid, down-regulates chemotaxis of selected

69 Together, these data demonstrate that endogenous opioids during mating induce neural plasticit

70 The endogenous opioid dynorphin B was evaluated for its role

71 and COOH-terminal functional domains of the endogenous opioid endomorphin-2 (EM-2) and the tachykini

72 a mu opioid agonist, mimicked the action of endogenous opioids, enhancing both mossy fiber LTP induc

73 differ functionally, is colocalized with the endogenous opioid ENK, and is not expressed by interstit

74 rt, we identified NT colocalization with the endogenous opioid enkephalin (ENK) in the RVM during the

75 The endogenous opioid enkephalin (ENK) was observed in about

76 ligand levels as well as mRNA levels of the endogenous opioid enkephalin (ENK-mRNA).

77 ed to enteric neurons immunoreactive for the endogenous opioid enkephalin, and 3) muOR immunoreactivi

78 In dorsal striatum, which expresses the endogenous opioid enkephalin, patches (or striosomes) ar

79 agents (e.g. morphine), or by the release of endogenous opioids following stressful procedures.

80 aches to pain management, such as harnessing endogenous opioids for pain relief.

81 approaches to pain management by harnessing endogenous opioids for pain relief.SIGNIFICANCE STATEMEN

82 lterations in both receptor availability and endogenous opioid function in CNBP that are relevant to

83 ayed pain was partly the result of increased endogenous opioid function, naloxone or naloxone methiod

84 n is consistent with the hypothesis that the endogenous opioids have a role in reducing the experienc

85 Endogenous opioids have been repeatedly shown to be invo

86 nd incentive value suggests that the role of endogenous opioids in reward processing does not depend

87 These findings led us to test the role of endogenous opioids in the A112G mice.

88 hat POMC neurons contribute to the action of endogenous opioids in the brain area during sexual behav

89 Evidence showing expression of endogenous opioids in the mammalian retina is sparse.

90 cancer were used to investigate the role of endogenous opioids in the modulation of pancreatic cance

91 mine cue-reactivity to elucidate the role of endogenous opioids in the neural systems underlying drug

92 and enkephalin peptides are the predominant endogenous opioids in the RAIC and their distinct distri

93 he hypotheses that mating-induced release of endogenous opioids in the VTA causes morphological chang

94 or antagonists, indicating a pivotal role of endogenous opioids in this process.

95 To help in understanding the function of endogenous opioids in this structure, we sought to ident

96 rexigenic peptides, neuropeptide Y (NPY) and endogenous opioids, in the arcuate nucleus of the hypoth

97 Endogenous opioids inhibit the onset and progression of

98 To determine whether NPY and endogenous opioids interact, we tested the hypothesis th

99 stained pain induced the regional release of endogenous opioids interacting with mu-opioid receptors

100 Blockade of endogenous opioid interaction using naltrexone (NTX) pro

101 These results indicate that an endogenous opioid is present and functions as a tonicall

102 e of tetra- and pentapeptides, including the endogenous opioids leucine enkephalin (Tyr-Gly-Gly-Phe-L

103 vasopressin administration, suggesting that endogenous opioids may be selectively engaged during the

104 with growing evidence that dysregulation of endogenous opioids may have an important role in the pat

105 This action of endogenous opioids may serve to counterbalance excitator

106 Such a receptor, due to the release of endogenous opioids, may have significant impact upon the

107 connection between allopregnanolone and the endogenous opioid mechanism.

108 responses that are more heavily regulated by endogenous opioid mechanisms, and the OPRM1 GA/GG genoty

109 oaches have shown that acupuncture activates endogenous opioid mechanisms.

110 Thus, endogenous opioids modulate resting ventilation, ventila

111 n impossible to unequivocally identify which endogenous opioids modulate the incentive value of rewar

112 To test whether endogenous opioids modulate these lamina II interneurons

113 MOR activation is a potential mechanism for endogenous opioid modulation of cholinergic activity.

114 suggest that repeated social stress engages endogenous opioid modulation of LC activity and induces

115 These data support the hypothesis that endogenous opioid modulation of organ development is a f

116 rom alterations in neurochemistry (dopamine, endogenous opioids), neuroanatomy (limbic system), and s

117 t evidence directly links the actions of the endogenous opioid neuropeptide dynorphin in modulating m

118 upled receptor family and the main target of endogenous opioid neuropeptides and morphine.

119 s) that mediate the physiological effects of endogenous opioid neuropeptides and opiate drugs such as

120 the individual capacity to acutely activate endogenous opioid neurotransmision under expectations of

121 Endogenous opioid neurotransmission activating mu-opioid

122 a significant role of estrogen in modulating endogenous opioid neurotransmission and associated psych

123 ith the neutral state, reflecting changes in endogenous opioid neurotransmission during the experienc

124 lability in vivo and a greater activation of endogenous opioid neurotransmission during the pain stre

125 associated with opposite responses of DA and endogenous opioid neurotransmission in a distributed net

126 sessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain reg

127 Variations in mu-opioid receptor-mediated endogenous opioid neurotransmission may underlie some of

128 These data demonstrate that endogenous opioid neurotransmission on mu-opioid recepto

129 d are further associated with activations in endogenous opioid neurotransmission, and as a trend cort

130 e introduces variability in MOR function and endogenous opioid neurotransmission.

131 ted to the experience of reward is linked to endogenous opioid neurotransmission.

132 IL-1 family cytokines interact with central endogenous opioid neurotransmitter systems, inducing or

133 hat is a physiologically relevant target for endogenous opioid neurotransmitters and analgesics, has

134 The endogenous opioid neurotransmitters and mu-opioid recept

135 These results indicate that an endogenous opioid, OGF, inhibits the onset and progressi

136 Opioid growth factor (OGF) is an endogenous opioid peptide ([Met(5)]enkephalin) that inte

137 ted by Derrick and Martinez to antagonism of endogenous opioid peptide action.

138 eatment with kelatorphan stabilizes putative endogenous opioid peptide agonists released by naloxone

139 sitive to antagonism by antisera against the endogenous opioid peptide beta-endorphin.

140 s affecting the efficacy of analogues of the endogenous opioid peptide dynorphin (Dyn) A have focused

141 They are activated by the endogenous opioid peptide dynorphin (DYN) and expressed

142 receptor (KOR) is the primary target for the endogenous opioid peptide dynorphin (DYN), and KORs resi

143 The structural properties of the endogenous opioid peptide dynorphin A(1-17) (DynA), a po

144 perties of chronic stress are encoded by the endogenous opioid peptide dynorphin acting on specific s

145 The endogenous opioid peptide endomorphin-1 (1) was modified

146 A decrease in endogenous opioid peptide inhibitory tone on the afterno

147 absence of dynorphin demonstrates that this endogenous opioid peptide mediates the dysphoric effects

148 amine receptors, can cause the release of an endogenous opioid peptide that binds to mu opioid recept

149 Beta-endorphin is an endogenous opioid peptide that is released during stress

150 Dynorphin A is an endogenous opioid peptide that produces non-opioid recep

151 An endogenous opioid peptide, [Met5]-enkephalin, termed opi

152 Expression of dynorphin, an endogenous opioid peptide, increases with age and has be

153 ose of kelatorphan, an inhibitor of multiple endogenous opioid peptide-degrading enzymes, stabilizes

154 Endogenous opioid peptides (EOPs) have been shown to pla

155 ce Tyr-Gly-Gly-Phe at the N terminus of most endogenous opioid peptides (EOPs).

156 icotine) would increase neurotransmission of endogenous opioid peptides (i.e., endorphins) in the nuc

157 ypothesis that exercise-induced increases in endogenous opioid peptides act in a manner similar to ch

158 These findings further suggest that endogenous opioid peptides activate mu opioid receptors

159 ation is a good assay for activation because endogenous opioid peptides all induce internalization.

160 receptors are the pharmacological targets of endogenous opioid peptides and morphine-like alkaloid dr

161 the present study was to examine the role of endogenous opioid peptides and opioid receptors specific

162 ce male rat sexual behavior, suggesting that endogenous opioid peptides are released during mating.

163 mu OR) mediates the physiological effects of endogenous opioid peptides as well as the structurally d

164 Accumulating evidence indicates that the endogenous opioid peptides dynorphinA-(1-17) and dynorph

165 trol of feeding, although roles for specific endogenous opioid peptides have barely been addressed.

166 ge mass spectrometry (LC-MS(3)) to determine endogenous opioid peptides in microdialysis samples coll

167 ric oxide (NO)-dependent neuronal release of endogenous opioid peptides in the central nervous system

168 We therefore suggest that endogenous opioid peptides may act as neuromodulators to

169 Protecting enkephalins, endogenous opioid peptides released in response to nocic

170 Endogenous opioid peptides serve as growth factors in de

171 studies emphasize complex interplays between endogenous opioid peptides targeting mu-receptors, such

172 NK) and leucine-enkephalin (L-ENK) are small endogenous opioid peptides that have been implicated in

173 The endomorphins represent a novel group of endogenous opioid peptides that have high affinity for t

174 gesting that estrogen induces the release of endogenous opioid peptides that in turn activate the MOR

175 gests that cocaine is causing the release of endogenous opioid peptides which activate mu opioid rece

176 Endogenous opioid peptides within the nucleus accumbens,

177 d to examine the effects of morphine and the endogenous opioid peptides, endomorphin-1 (EM-1) and end

178 ioid receptor (MOP) is activated by numerous endogenous opioid peptides, remains an attractive therap

179 atible with the presence of raised levels of endogenous opioid peptides.

180 H modulates the production and/or release of endogenous opioid peptides.

181 e the same as the stimulatory effects of the endogenous opioid peptides.

182 Although studies suggest that endogenous opioids play a role in immune regulation in a

183 To enhance beta-endorphin (BEP), the endogenous opioid polypeptide that boosts immune activit

184 igm, which is known to induce the release of endogenous opioids, produced greater antinociception in

185 In an investigation of whether endogenous opioid receptor-activation reduces ischemic i

186 pa opioid receptor signaling, and converting endogenous opioid receptor-mediated hyperalgesia to anal

187 uration of diabetes and that intervention of endogenous opioid-receptor interfacing with an opioid an

188 The present findings provide evidence that endogenous opioids regulate LC neuronal activity during

189 Here, we used PET to show that endogenous opioid release after social laughter may prov

190 It has been proposed that endogenous opioid release after social laughter would pr

191 may be in part mediated via inhibition of an endogenous opioid release as well as blockade of the unw

192 Because LC activation is tempered by endogenous opioid release during stress, the magnitude o

193 1)C]carfentanil to quantify laughter-induced endogenous opioid release in 12 healthy males.

194 uring rejection, MDD patients showed reduced endogenous opioid release in brain regions regulating st

195 Overall, the results suggest that endogenous opioid release in core affective brain region

196 that oral amphetamine administration induces endogenous opioid release in different areas of human br

197 whether feeding results in hedonia-dependent endogenous opioid release in humans.

198 remains unresolved whether feeding leads to endogenous opioid release in humans.

199 o characterize baseline MOR availability and endogenous opioid release in pathological gamblers (PG)

200 study provides the first evidence of blunted endogenous opioid release in PG.

201 creased pleasurable sensations and triggered endogenous opioid release in thalamus, caudate nucleus,

202 Endogenous opioid release in the dorsal ACC and PAG was

203 o demonstrate a pharmacologically stimulated endogenous opioid release in the living human brain by e

204 vation, which was positively correlated with endogenous opioid release in the nucleus accumbens, a re

205 Placebo-induced endogenous opioid release in these regions was associate

206 s local release of glutamate that results in endogenous opioid release through the activation of peri

207 Feeding induced significant endogenous opioid release throughout the brain.

208 Endogenous opioid release was stronger after laughter ve

209 hesis that MOR system activation (reflecting endogenous opioid release) in response to social rejecti

210 Feeding led to significant endogenous opioid release, and this occurred also in the

211 These observations, consistent with endogenous opioid release, highlight the role of the mu-

212 g that progesterone blocked estrogen-induced endogenous opioid release, relieving estrogen inhibition

213 d upon data showing the stereoselectivity of endogenous opioid release.

214 we found no effect of A118G on pain-induced endogenous opioid release.

215 of placebo analgesia is the potentiation of endogenous opioid responses to noxious stimuli.

216 Finally, given evidence that endogenous opioids restrain stress-induced LC activation

217 Endogenous opioid signaling functions as part of a compl

218 Endogenous opioid signaling in the ACC appears to be bot

219 Endogenous opioid signaling in the anterior cingulate co

220 However, much research suggests that endogenous opioid signaling underlies the hedonic aspect

221 by other opiate drugs such as methadone and endogenous opioids such as endorphins.

222 ith mu-opioid receptor BPND and pain-induced endogenous opioid system activation in the amygdala, fur

223 with the Dissociative Experiences Scale and endogenous opioid system activation with the Barratt Imp

224 ssociated with greater reductions in BP(ND) (endogenous opioid system activation) in the patient grou

225 or concentrations and greater stress-induced endogenous opioid system activation.

226 tivity analyses on individual differences in endogenous opioid system activity revealed that placebo

227 The authors investigated the role of the endogenous opioid system and mu-opioid receptors in emot

228 The endogenous opioid system and opioid mu receptors (mu-rec

229 with alterations in the responsivity of the endogenous opioid system and the hypothalamic-pituitary-

230 In conclusion, modulation of the endogenous opioid system by TGF-beta signaling improves

231 Patients showed evidence of endogenous opioid system deactivation in the left nucleu

232 hese findings indicate the importance of the endogenous opioid system for the maintenance of immunity

233 riatal D2/D3R function, which, together with endogenous opioid system function, contribute to the sen

234 Our results demonstrate heterogeneity in endogenous opioid system functional measures across pain

235 ity and affective state, but also with brain endogenous opioid system functional measures.

236 The endogenous opioid system has been implicated in sexual b

237 The endogenous opioid system has been implicated in the medi

238 The endogenous opioid system has been shown to regulate soci

239 etween ethanol (EtOH) administration and the endogenous opioid system has been studied for many years

240 beta, IL-1ra, and functional measures of the endogenous opioid system in 34 healthy volunteers, in th

241 of this study was to assess the role of the endogenous opioid system in delaying the onset of pain i

242 nt with an inhibitory/anxiolytic role of the endogenous opioid system in limbic regions of the tempor

243 cal and clinical studies have implicated the endogenous opioid system in major depression and in the

244 This study investigated the role of the endogenous opioid system in maternal and affiliative beh

245 rocedure to evaluate the responsivity of the endogenous opioid system in nicotine-dependent individua

246 se results may suggest an involvement of the endogenous opioid system in some of the multitude of eff

247 administration (SA) and dysregulation of the endogenous opioid system in the nucleus accumbens shell

248 The endogenous opioid system is involved in modulating the e

249 The endogenous opioid system is involved in stress responses

250 The endogenous opioid system of the brain has been implicate

251 es, we directly examined the activity of the endogenous opioid system on mu-opioid receptors in human

252 mu-opioid receptor concentrations and in the endogenous opioid system response to a negative emotiona

253 The endogenous opioid system supports a multitude of functio

254 al opioid release.SIGNIFICANCE STATEMENT The endogenous opioid system supports both hedonic and homeo

255 e suggest that Caenorhabditis elegans has an endogenous opioid system that acts through NPR-17, and t

256 -induced feeding in rats was mediated by the endogenous opioid system through systemic administration

257 l research analyses in which elements of the endogenous opioid system were frequently in the vanguard

258 oreover, Tat expression widely disrupted the endogenous opioid system, altering mu and kappa, but not

259 Evidence points to the endogenous opioid system, and the mu-opioid receptor (MO

260 Neurotrophins modulate the endogenous opioid system, but the underlying mechanisms

261 through the activation of NF-kappaB and the endogenous opioid system, enhances HCV replicon expressi

262 The endogenous opioid system, which alleviates physical pain

263 rat colitis and hypertension models via the endogenous opioid system.

264 sized to be mediated by the pain-suppressive endogenous opioid system.

265 T-KO mice, confirming the involvement of the endogenous opioid system.

266 mbs and which was partially dependent on the endogenous opioid system.

267 as been associated with dysregulation of the endogenous opioid system.

268 treat diseases involving dysfunction of the endogenous opioid system.

269 vous system (CNS) overlap significantly with endogenous opioid systems and can be dually targeted.

270 Furthermore, we will explore the endogenous opioid systems and novel cancer pain therapeu

271 f a new CB receptor differentially linked to endogenous opioid systems based upon data showing the st

272 The interaction between the stress axis and endogenous opioid systems has gained substantial attenti

273 The interaction between the stress axis and endogenous opioid systems has gained substantial clinica

274 altrexone, indicating an additional role for endogenous opioid systems in regulation of the PVN respo

275 itter/neuromodulator, acting in concert with endogenous opioid systems to regulate analgesic response

276 However, there is evidence that endogenous opioid systems within this brain reward circu

277 is system resides in its ability to regulate endogenous opioid systems, making it a potential target

278 l behaviors in other species are mediated by endogenous opioid systems, opiate regulation of pair bon

279 action with the mesolimbic dopamine (DA) and endogenous opioid systems.

280 Endogenous opioids target noradrenergic locus ceruleus (

281 estrogen treatment stimulates the release of endogenous opioids that activate mu-OR in the limbic sys

282 We suggest that any endogenous opioids that are released by noxious stimuli

283 to induce analgesia in rat pups by releasing endogenous opioids that bind to mu opioid receptors in t

284 hosphorylation, an effect also manifested by endogenous opioids that is reflected by the ability of a

285 Enkephalins (ENKs) are endogenous opioids that regulate synaptic excitability o

286 ate and neural activation as well as altered endogenous opioid tone in the differential response to a

287 ondition, however, significant reductions in endogenous opioid tone were observed at the level of tha

288 sceral pain, raising the question of whether endogenous opioids tonically modulate the pain of viscer

289 data suggest that upshifts and downshifts in endogenous opioid transmission in the BLA mediate the en

290 What remains unknown, however, is whether endogenous opioid transmission within the PFC modulates

291 the analgesic effectiveness of exogenous and endogenous opioids under pathological pain conditions.

292 The phenotype of mice lacking both endogenous opioids was nearly identical to the phenotype

293 es on mu-opioid receptor (MOR) activation by endogenous opioids, we measured MOR-1 internalization in

294 amined the effect of endomorphin-1 (EM1), an endogenous opioid with a high affinity for the mu opiate

295 The endomorphins are endogenous opioids with high affinity and selectivity fo

296 Endomorphin-1 and -2 (EM1, EM2) are endogenous opioids with high affinity and selectivity fo

297 sident-intruder testing to determine whether endogenous opioids within brain motivational circuitry m

298 provide evidence for a functional release of endogenous opioids within the LC.

299 e severe the RLS, the greater the release of endogenous opioids within the medial pain system.

300 n strong painful stimuli, the recruitment of endogenous opioids works to close this gate, reducing ov