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1 or lacking either pre-pro-enkephalin or beta-endorphin.
2 yloid fiber formed by the human hormone beta-endorphin.
3 ltered cleavage profile for the peptide beta-endorphin.
4 a-neoendorphin, but not endomorphins or beta-endorphin.
5 cyte-stimulating hormone (beta-MSH) and beta-endorphin.
6 beta-lipotropin to gamma-lipotropin and beta-endorphin.
7 in the level of C-terminally processed beta-endorphin.
8 sed for dual immunocytochemistry of Fos/beta-endorphin.
9 gh the post-translational processing of beta-endorphin.
10 MC), or PVN levels of Met-Enkephalin or beta-Endorphin.
11 beta-lipotropic hormone (beta LPH), and beta endorphin.
12 de Y, vasoactive intestinal peptide, or beta-endorphin.
13 ulating hormone, and the opioid peptide beta-endorphin.
14 acid decarboxylase 67 (GAD67), NPY, and beta-endorphin.
15 duced increases in nitrite, nitrate and beta-endorphin.
16 ate an NO-dependent neuronal release of beta-endorphin.
17 abolites nitrite and nitrate as well as beta-endorphin.
18 for their content of NO metabolites and beta-endorphin.
19 a against the endogenous opioid peptide beta-endorphin.
20 as methadone and endogenous opioids such as endorphins.
21 imulating hormone, beta-lipotrophin, and the endorphins.
22 s well as to endogenous peptide ligands like endorphins.
24 tidase which converts beta-endorphin to beta-endorphin 1-17 (gamma-endorphin), beta-endorphin 1-18, a
25 beta-endorphin 1-17 (gamma-endorphin), beta-endorphin 1-18, and their corresponding C-terminal fragm
26 ministration of morphine (1 microg) and beta-endorphin (1 microg) into either the amygdala alone or t
28 rphine (1 microg) into the amygdala and beta-endorphin (1 microg) into the PAG failed to produce inte
29 milar effects of intra-DVC injection of beta-endorphin (1 pmol) are inhibited by naloxone and not by
30 n (epsilon)-opioid-receptor antagonist, beta-endorphin(1-27) prevents these effects of etorphine.
31 one (LAAM), morphine, meperidine, DADL, beta-endorphin(1-31), enkephalins, and dynorphin A(1-17) prod
32 o the suppressive actions of Gly-Gln or beta-endorphin-(1-27) injections that modulate voluntary etha
33 y was shown to be comparable to central beta-endorphin-(1-27) or intraperitoneal (i.p.) naltrexone-in
34 ontrast, the opioid peptidergic agonist beta-endorphin (10 microgram/kg, i.p.) administered after the
35 Following intrathecal administration, beta-endorphin (10-100 nmol) and GRP (1-10 nmol) dose-depende
36 is of fluorogenic peptides based on the beta-endorphin 12-24 sequence, Abz-T-P-L-V-T-L-X(1)-X(2)-N-A-
37 he rostral ventromedial medulla altered beta-endorphin (15 microg) analgesia elicited from the ventro
38 Both morphine (2.5-5 micrograms) and beta-endorphin (2.5-5 micrograms) microinjected into either t
40 investigated whether glycyl-glutamine (beta-endorphin(30-31)), an inhibitory dipeptide synthesized f
41 ffective in reducing morphine (60%) and beta-endorphin (79%) analgesia in the amygdala on the jump te
42 pro-opiomelanocortin, the precursor of beta-endorphin (a known EOP), and constituted the majority of
43 the DVC, whereas the similar effects of beta-endorphin, a peptide derived from the same precursor, ar
49 t as well as more rapid dissociation of beta-endorphin amyloid fibrils at lower pH indicate the contr
53 exercise increases blood levels of both beta-endorphin (an opioid) and anandamide (an endocannabinoid
54 wever, the A118G variant receptor binds beta-endorphin, an endogenous opioid that activates the mu op
57 significantly reduced morphine, but not beta-endorphin analgesia in the amygdala on the tail-flick te
58 ultiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, and in terms of whether
60 Whereas mecamylamine failed to reduce beta-endorphin analgesia on either measure, scopolamine produ
61 %) and transient (30 min) reductions in beta-endorphin analgesia on the jump test, MK-801 produced mi
64 es with mice confirm that these glycosylated endorphin analogues are potential drug candidates that p
67 es in the helical address region of the beta-endorphin analogues without destroying mu-, delta-, or k
68 gy states are suggested for the glycosylated endorphin analogues, a flexible aqueous state and a rest
69 owed colocalization of cathepsin L with beta-endorphin and alpha-MSH in the intermediate pituitary an
70 tion, mediated by the hedonic action of beta-endorphin and anhedonic effects of withdrawal, may theor
73 measurement of instrumental behavior of beta-endorphin and enkephalin knock-out mice that both opioid
75 nules yet expresses endogenous opioids (beta-endorphin and Met-enkephalin) and uroguanylin in apical
76 ors (MOR, OPRM1) mediate the effects of beta-endorphin and modulate many biological functions includi
79 try and immunoelectron microscopy using beta-endorphin and mu-opiate receptor specific antibodies.
81 ) neurons release the endogenous opioid beta-endorphin and POMC neuron activity is inhibited by opioi
82 infiltration of immunocytes containing beta-endorphin and the consequent decrease of the beta-endorp
84 ver, neurons triple-labeled with c-Fos, beta-endorphin and VGLUT3 were noted in this region following
86 pletely prevented carboxy-shortening of beta-endorphins and greatly diminished conversion of beta-lip
87 n MRM transitions for alpha-endorphin, gamma-endorphin, and [D-Ala(2)]-gamma-endorphin were m/z 873.6
88 euroendocrine peptides (dynorphin A-17, beta-endorphin, and alpha- melanocyte-stimulating hormone) in
89 nes adrenocorticotropic hormone (ACTH), beta-endorphin, and alpha-melanocyte stimulating hormone (alp
90 cathepsin L in the production of ACTH, beta-endorphin, and alpha-MSH peptide hormones in the regulat
91 ut mice showed major decreases in ACTH, beta-endorphin, and alpha-MSH that were reduced to 23, 18, an
93 ropin-releasing hormone (GnRH), VP, OT, beta-endorphin, and dopamine neurons, are responsive to mu-re
94 iomelanocortin (POMC), the precursor to beta-endorphin, and endomorphin 1 and 2 on sectioned rat fore
95 ioid receptor agonists (e.g., morphine, beta-endorphin, and enkephalin) inhibit luteinizing hormone (
96 dotropin-releasing hormone-I, dopamine, beta-endorphin, and gonadotropin-releasing hormone-II neurons
97 gesic responses induced by morphine and beta-endorphin, and indicate that the latter response is medi
98 actin, corticotropin-releasing hormone, beta-endorphin, and somatotropin release-inhibiting factor.
99 as well as its derivatives beta LPH and beta-endorphin, and that this process is modulated by TPA, IL
101 ived feeding states but were reduced in beta-endorphin- and enkephalin-deficient mice only when they
102 nmol) dose-dependently attenuates both beta-endorphin- and GRP-elicited robust scratching without af
104 ted for three different receptors: anti-beta-endorphin anti-body, streptavidin, and thrombin, and the
105 n, growth hormone releasing factor, and beta-endorphin are nearly equivalent substrates for the enzym
108 ng a monoclonal antibody (3E-7) against beta-endorphin as a target, we selected a single peptide with
109 ntial affinity to the endogenous ligand beta-endorphin as well as alterations in pain sensitivity, dr
112 in pain modulation-metenkephalin (ME), beta-endorphin (BE), and substance P (SP)-in patients undergo
113 Within 36 h after TPA stimulation, beta-endorphin became undetectable in cell extracts, coincidi
117 leasing hormone (CRH), urocortin (Ucn), beta-endorphin (beta-END), ACTH, and corticosterone (CORT) or
119 The enzymatic cleavage products of beta-endorphin (beta-endorphin1-27 and Gly-Gln) reduce volunt
121 The mechanism by which ethanol induces beta-endorphin (beta-EP) neuronal death during the developmen
122 system is involved in ethanol-regulated beta-endorphin (beta-EP) release from rat hypothalamic neuron
123 beta-endorphin to beta-endorphin 1-17 (gamma-endorphin), beta-endorphin 1-18, and their corresponding
124 ced by the mu-sensitive opioid peptide, beta-endorphin (betaEND, 10 microg, i.c.v.) was significantly
125 CB1R activation selectively increases beta-endorphin but not alpha-melanocyte-stimulating hormone r
128 of cell bodies containing enkephalin or beta-endorphin, colchicine (90-100 microg/kg) was injected in
129 G) may have higher receptor binding for beta-endorphin compared with AA homozygotes that may contribu
130 of oxidation products of NO as well as beta-endorphin, compared to levels in fractions collected und
131 in arterial pressure elicited by i.c.v. beta-endorphin, consistent with evidence that cyclic dipeptid
133 y, CB(2) immunolabeling was detected on beta-endorphin-containing keratinocytes in stratum granulosum
135 peritoneally twice at 3 h intervals, and the endorphin content of microdialysates was analyzed by a s
136 though conversion of beta-lipotropin to beta-endorphin decreased, the lack of PC2 activity caused an
140 e aggressive conspecific several of the beta-endorphin deficient mice showed clear signs of counter a
144 in proenkephalin knockout (PENK KO) and beta-endorphin-deficient (BEND KO) mice, and how the body wei
145 Herein we demonstrate that morphine and beta-endorphin disrupt this long-range synchrony of gamma osc
146 allenge the dogma that shorter forms of beta-endorphin do not exhibit receptor activity; we show that
148 u and kappa opioid receptors as well as beta-endorphin each produce analgesia elicited from the amygd
149 ies have demonstrated that morphine and beta-endorphin employ different anatomical and neurochemical
151 d neurons double-labeled with c-Fos and beta-endorphin, enkephalin or VGLUT3 in the ARC were signific
152 er, growth hormone releasing factor and beta-endorphin exhibit a 40-fold higher kcat, but a 10-fold d
153 nic mice with a selective deficiency of beta-endorphin exhibit normal analgesia in response to morphi
155 beta-endorphin), heterozygous mice (50% beta-endorphin expression) and sibling wildtype mice from the
156 as an acidic pH but, on exocytosis, the beta-endorphin fibril would encounter neutral pH conditions (
159 eptor activation induces the release of beta-endorphin from keratinocytes and the activation of G-pro
161 sor-to-product ion MRM transitions for alpha-endorphin, gamma-endorphin, and [D-Ala(2)]-gamma-endorph
162 h the rank order of etorphine > DAMGO = beta-endorphin > morphine > butorphanol, and the affinity of
165 ting hormone; and the endogenous opioid beta-endorphin) have a diverse array of biological activities
166 ozygous knockout mice (entirely lacking beta-endorphin), heterozygous mice (50% beta-endorphin expres
169 beta-endorphin immunostaining, whereas beta-endorphin-immunoreactive neurons were absent in retinas
170 xtracts, coinciding with an increase of beta-endorphin-immunoreactive protein in the culture medium.
171 significant increases in POMC mRNA and beta-endorphin immunoreactivity in both ipsilateral and contr
172 ressing amacrine cells was positive for beta-endorphin immunostaining, whereas beta-endorphin-immunor
175 ed secretion of both chromogranin A and beta-endorphin in response to the usual secretagogue, cortico
177 nalgesia elicited by either morphine or beta-endorphin in the amygdala could be altered by either the
178 omelanocortin (POMC) neurons to release beta-endorphin in the arcuate nucleus (ARC) of the hypothalam
180 hat enhancement of endogenous levels of beta-endorphin in the hypothalamus via beta-endorphin neuron
181 on of AAS also increased the content of beta-endorphin in the midline thalamus, suggesting a possible
182 but decreased the potency of the opioid beta-endorphin in the periaqueductal gray region of the midbr
184 adiation, to date a functional role for beta-endorphin in the regulation of human epidermal melanocyt
185 lanocyte-stimulating hormone (MSH), and beta-endorphin in the regulation of skin pigmentation, and a
186 he data do not support a major role for beta-endorphin in the regulation of sleep or social stress-in
187 ivates neurons containing enkephalin or beta-endorphin in the rVLM as well as in the periaqueductal g
188 rphin were used to study the release of beta-endorphin in the urethane anaesthetized rat following el
190 ation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to oxidation of methionine r
193 ndogenous concentrations of alpha- and gamma-endorphins in rat brains were 13.8+/-0.57 (mean+/-SD; n=
194 eficient mice were used to study the role of endorphins in the acute physiological and behavioral res
195 transiently elevated extracellular levels of endorphins in the nucleus accumbens, whereas nicotine an
198 produced a dose-dependent inhibition of beta-endorphin-induced hypotension, but not bradycardia, with
201 administration of subthreshold doses of beta-endorphin into both structures also results in a profoun
202 doses of morphine into both structures, beta-endorphin into both structures, morphine into one struct
205 ctures, morphine into one structure and beta-endorphin into the other structure, or morphine and beta
210 l stimulus was applied, suggesting that beta-endorphin is necessary for CB(2) receptor-mediated antin
214 rodents, another POMC-derived peptide, beta-endorphin, is coordinately synthesized in skin, elevatin
215 e and behavioral effects were absent in beta-endorphin knockout mice and in mice lacking p53-mediated
216 An antibody that selectively recognized beta-endorphin labeled fibers and neurons in the ventral horn
217 used an increase in beta-lipotropin and beta-endorphin levels in the mutant animals, but no increases
220 reatening episodes implicates increased beta-endorphin levels resulting from acid-mediated esophageal
222 en, dyadic satisfaction correlated with beta-endorphin levels, depression, and perception of illness.
225 ypothesize that this drug-induced release of endorphins may contribute to the positive reinforcing an
227 itary chemosensory cells that coexpress beta-endorphin, Met-enkephalin, uroguanylin, and Trpm5 exist
228 In conclusion, the results suggest that beta-endorphin modulates the acute endocrine, thermoregulator
230 sal links for itch-eliciting effects by beta-endorphin-MOP receptor and GRP-BB2 receptor systems and
231 roM concentrations of etorphine, DAMGO, beta-endorphin, morphine, and butorphanol, DAMGO-stimulated G
232 igned to examine the involvement of the beta-endorphin/mu-opiate receptor system in human epidermal m
233 cortin-1 receptor, we conclude that the beta-endorphin/mu-opiate receptor system participates in the
235 beta-endorphin in the hypothalamus via beta-endorphin neuron transplantation suppresses stress respo
237 sition of the complement protein C1q in beta-endorphin neuronal cells in both in vitro and in vivo sy
238 lates exosome-mediated, ethanol-induced beta-endorphin neuronal death.SIGNIFICANCE STATEMENT Neurotox
239 treatments increased the number and the beta-endorphin neuronal killing activity of microglial exosom
240 2.6%, depending on neuronal location), beta-endorphin neurons (68.3.0 +/- 4.4%), and VP neurons (41-
243 to traditional mu and kappa opioids and beta-endorphin, none of the OFQ/N fragments in the amygdala e
248 D can improve the sequence coverage for beta-endorphin over performing ECD alone (i.e., from 72 to 97
249 orks) to show that three neuropeptides (beta-endorphin, oxytocin, and dopamine) play particularly imp
252 piomelanocortin (POMC) neuron-producing beta-endorphin peptides in the hypothalamus in a postnatal ra
255 n inhibitory dipeptide synthesized from beta-endorphin post-translationally, inhibits IL-1beta and PG
256 V8 expressing the analgesic gene prepro-beta-endorphin (ppbetaEP) led to significant (P < 0.0001) rev
257 for insulin-degrading enzyme as both a beta-endorphin-processing and -inactivating enzyme is implica
258 experiments tested the hypothesis that beta-endorphin-producing neurons, that is, proopiomelanocorti
259 c acid (GABA), neuropeptide Y (NPY), or beta-endorphin receptor blockade in the ipsilateral hypothala
260 ascular reflexes through enkephalin- or beta-endorphin-related opioid receptors in the rostral ventro
261 ature, at least in part, by stimulating beta-endorphin release from pro-opiomelanocortin neurons that
266 , sensation, plasma levels of cortisol, beta-endorphin, selected gut neuropeptides, norepinephrine, e
267 keratinocytes, subsequently increasing beta-endorphin signaling at opioid receptors, and produces an
269 (tail-flick: 70-75%; jump: 60-81%) and beta-endorphin (tail-flick: 100%; jump: 93%) analgesia elicit
270 lpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines n
271 hormone (alpha-Msh) and carboxy-cleaved beta-endorphin, the products of Cpe-dependent processing of P
272 shown the distribution of dynorphin and beta-endorphin throughout social behavior circuits within the
273 ine contains a peptidase which converts beta-endorphin to beta-endorphin 1-17 (gamma-endorphin), beta
274 attachment, binding of the neuropeptide beta-endorphin to mu-opioid receptors in the central nervous
275 ne regulating feeding behavior, whereas beta-endorphin underlies orosensory reward in high need state
276 geting mu-receptors, such as enkephalins and endorphins, underlying the regulation of feeding and bod
283 d in rats when naloxone or antiserum to beta-endorphin was injected in the hindpaw where the noxious
285 mity to fibers containing enkephalin or beta-endorphin, was observed in the rVLM and ventrolateral PA
286 ate an NO-dependent neuronal release of beta-endorphin, we conducted a ventricular-cisternal perfusio
287 en the powerful analgesic properties of beta-endorphin, we tested this hypothesis using pain toleranc
288 tern blot analysis, POMC, beta LPH, and beta-endorphin were detected in cell extracts under baseline
290 rphin, gamma-endorphin, and [D-Ala(2)]-gamma-endorphin were m/z 873.6-->429.6; 929.6-->542.3; 936.6--
292 d antibodies to the carboxy-terminus of beta-endorphin were used to study the release of beta-endorph
293 chanism allows for the local release of beta-endorphin, where CB(2) receptors are present, leading to
294 y to inflamed sites, where they release beta-endorphin which activates peripheral opioid receptors to
295 timulates release from keratinocytes of beta-endorphin, which acts at local neuronal mu-opioid recept
296 and exercise both induce the release of beta-endorphin, which plays an important role in the modulati
298 keratinocytes of the endogenous opioid beta-endorphin, which then acts at opioid receptors on primar
299 There was no correlation of IL-1 or beta-endorphin with any psychosocial or behavioral compliance