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1 gonist-mediated down-regulation of the delta opiate receptor.
2  GIRK channels may mediate the actions of mu opiate receptors.
3 r (CRF), and endogenous opioids acting at mu-opiate receptors.
4  recent developments in our understanding of opiate receptors.
5 ion channel that is selectively modulated by opiate receptors.
6  bound to 125I-Tyr-MIF-1 were not endogenous opiate receptors.
7 ta and micro but not kappa G protein-coupled opiate receptors.
8  of spinal cord kappa and delta (but not mu) opiate receptors.
9 ting that the analgesia was mediated through opiate receptors.
10 ssary for release to be directly adjacent to opiate receptors.
11 ars striking amino acid sequence homology to opiate receptors.
12 at exhibits a high selectivity for the delta-opiate receptors.
13 ne, indicating the presence of functional mu-opiate receptors.
14 pha(i3)/betagamma/AGS3 appears to mediate mu opiate receptor activation of PKA signaling as well as h
15               These data indicate that delta opiate receptor activity is a prerequisite for the manif
16 o their decreased dopaminergic modulation of opiate receptor activity.
17 ther hallucinogens and consistent with kappa opiate receptor agonism.
18 lary OFF cells modulate BAT activity, the mu-opiate receptor agonist (d-Ala2, N-Me-Phe4, Gly-ol5)-enk
19 tion is increased in neuronal tissue by a mu-opiate receptor agonist and it is proposed that endogeno
20                               Loperamide, an opiate receptor agonist, does not cross the blood-brain
21  others have used intrathecal fentanyl, a mu-opiate receptor agonist, in humans to reduce the input f
22 ry previously reported that the mu-selective opiate receptor agonist, sufentanil, produces a naloxone
23 diated EPSCs are blocked by the analgesic mu-opiate-receptor agonist Damgo and spinal blockade of bot
24 le melanocytes (HFM) express mRNA for the mu-opiate receptor and POMC.
25 ave high affinity and selectivity for the mu-opiate receptor and potent analgesic activity.
26 f any data showing cross-talk between the mu-opiate receptor and the melanocortin-1 receptor, we conc
27 se-dependent manner by microinjection of the opiate receptor antagonist methylnaloxonium into BLC.
28 ng the effect of local administration of the opiate receptor antagonist methylnaloxonium on heroin se
29                   High concentrations of the opiate receptor antagonist naltrexone did not block the
30   Anti-TGF-beta Ab as well as naltrexone (an opiate receptor antagonist) inhibited morphine-induced m
31                  In addition, naltrexone, an opiate receptor antagonist, abrogated the enhancing effe
32  SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect
33 ndent manner by the microinjection of the mu-opiate receptor antagonist, methylnaloxonium, into nPf.
34  carbachol-induced motor inhibition while an opiate receptor antagonist, naloxone, was microiontophor
35 onaltrexone (cyclofoxy, CF), a mu- and kappa-opiate receptor antagonist.
36 s of opiates with systemic administration of opiate receptor antagonists results in an increase in he
37 ecretogogues, and peripherally restricted mu-opiate receptor antagonists, the latter a major advance
38 rthermore, beta-END and its high affinity mu-opiate receptor are expressed at the protein level in gl
39 on, we have shown that beta-endorphin and mu-opiate receptor are expressed at the protein level in si
40 ved from the same precursor, are mediated by opiate receptors at the same site.
41                                              Opiate receptor avidity (B(max)'/K(D)) was measured in f
42                                              Opiate receptor avidity was found to be reduced by 30-35
43                                              Opiate receptor avidity was found to be significantly hi
44                        A uniform decrease of opiate receptor binding was found throughout the dorsal
45 gion in blood-brain barrier (BBB) transport, opiate receptor binding, and analgesia.
46 e delta (enkephalins) and kappa (dynorphins) opiate receptors, but none has been found to have any pr
47 n serotonergic transporters and occupancy of opiate receptors by substitute drugs (e.g. methadone and
48          These data suggest that this new mu opiate receptor cDNA encodes the mu 3 opiate receptor, s
49  opiate drugs with an affinity for the delta-opiate receptor confer similar protection.
50 e generated a number of mutants of the delta opiate receptor COOH-terminal tail.
51 The expression of both beta-endorphin and mu-opiate receptor correlated positively with their differe
52                 An increase of mu- and kappa-opiate receptor densities in specific brain regions may
53 eceptor-dependent reward pathway, or a kappa-opiate receptor-dependent aversion pathway, directly wit
54 ivational signaling is mediated through a mu-opiate receptor-dependent reward pathway, or a kappa-opi
55        Agonists for the mu, delta, and kappa opiate receptors did not change the binding, indicating
56                 One gene, OPRL1, encoding an opiate receptor, displayed extremely efficient levels of
57      In the natural killer (NK) cells, delta-opiate receptor (DOR) and mu-opioid receptor (MOR) inter
58               The molecular mechanism of the opiate receptor down-regulation is not known.
59  the changes in the density of mu- and kappa-opiate receptors during PST, as revealed by quantitative
60 ngle-channel patch-clamp recordings to study opiate receptor effects on dissociated neurons from rat
61 ngle-channel patch-clamp recordings to study opiate receptor effects on freshly dissociated neurons f
62 ariant of the previously characterized mu(3) opiate receptor-encoding mRNA.
63 is indicated significant expression of mu(3) opiate receptor-encoding RNA by undifferentiated human M
64               Morphine produces analgesia at opiate receptors expressed in nociceptive circuits.
65 vel, alternatively spliced variant of the mu opiate receptor gene.
66 of genomic sequence on 6q24-q25, near the mu opiate receptor gene.
67      We produced homologous, recombinant mu, opiate receptor, heterozygous and homozygous knockout an
68 dogenous opioid-peptide interactions with mu opiate receptors in normal nociceptive processing.
69               These results demonstrate that opiate receptors in parts of the extended amygdala may b
70 cate endogenous opioid-peptide actions at mu opiate receptors in several tests of nociceptive respons
71 cross the BBB, allowing it to gain access to opiate receptors in the CNS to produce a centrally media
72                                Activation of opiate receptors in the NAc dissociates G(i/o) into alph
73 strated the involvement of spinal cord kappa opiate receptors in this phenomenon.
74            Blockade of spinal kappa or delta opiate receptors, individually, can abolish the antinoci
75 (SA)-a highly selective agonist at the kappa opiate receptor-is believed to be one of the most potent
76 C is also innervated by the endogenous kappa-opiate receptor (kappa-OR) ligand dynorphin and expresse
77                               The endogenous opiate receptor-like 1 ligand, orphanin FQ (OFQ), which
78 ciceptin/orphanin FQ (Noc) and its receptor [opiate receptor-like receptor (ORL-1)] are highly expres
79                            Ligands of the mu-opiate receptor (MOR) are known to influence many functi
80                     Opiates active at the mu-opiate receptor (MOR) produce antinociception, in part,
81  the postsynaptic signaling mechanisms of mu-opiate receptors (MORs) and CB1 receptors in primary NAc
82 This study demonstrated the expression of mu-opiate receptor mRNA in cultured epidermal melanocytes,
83 from our laboratory have revealed a novel mu opiate receptor, mu 3, which is expressed in both vascul
84 ls and between mouse strains in levels of mu opiate receptor (muOR) expression, responses to painful
85 and primordial regulatory role of mu(3)-like opiate receptor/NO signaling in embryogenesis.
86 rmine whether a functionally competent mu(3) opiate receptor/NO-coupled regulatory pathway exists in
87 validating evidence of functional mu(3)-like opiate receptor/NO-coupled signaling within primary cult
88 enous opioid with a high affinity for the mu opiate receptor, on conditioned defeat.
89              Cannabinoid, dopamine (DA), and opiate receptor pathways play integrative roles in emoti
90                        Phosphorylation of mu opiate receptor protein is also enhanced approximately 5
91                   Phosphorylation of this mu opiate receptor protein was enhanced approximately 5-fol
92 ity was found to be reduced by 30-35% in the opiate-receptor rich areas of caudate, anterior putamen,
93 trathecal (i.t.) administration of the delta opiate receptor-selective antagonists naltrindole (NTI),
94 new mu opiate receptor cDNA encodes the mu 3 opiate receptor, since it exhibits biochemical character
95 unoelectron microscopy using beta-END and mu-opiate receptor specific antibodies and a functional rol
96 ctron microscopy using beta-endorphin and mu-opiate receptor specific antibodies.
97 mic morphine exposure requires a decrease in opiate receptor stimulation in the VTA and can be reliev
98 lly authentic, l-morphine, its cognate mu(3) opiate receptor subtype, and constitutive NO synthase.
99  signaling since these cells express the mu3 opiate receptor subtype.
100  It has been demonstrated that a specific mu-opiate-receptor subtype, mu3, mediates these downregulat
101                         mu, delta, and kappa opiate receptor subtypes are expressed in circuits that
102 ine the involvement of the beta-endorphin/mu-opiate receptor system in human epidermal melanocytes.
103 o examine the involvement of the beta-END/mu-opiate receptor system in human follicular melanocyte bi
104 ptor, we conclude that the beta-endorphin/mu-opiate receptor system participates in the regulation of
105 ure in humans is an enhancement of the brain opiate receptor system.
106 xpress a fully functioning beta-endorphin/mu-opiate receptor system.
107 nervated by the orexin neurons express kappa opiate receptors, the main receptor for dynorphin.
108                                           mu opiate receptors, the principal sites for opiate analges
109 ing effect on the response of the endogenous opiate receptor to the agonist D-alanine-5-leucine-enkep
110 nduced macrophage apoptosis proceeds through opiate receptors via P38 MAPK phosphorylation.
111 ominantly N-type calcium channels coupled to opiate receptors via PTX-sensitive (Gi/o) inhibitory G p
112 t this trapping was not caused by binding to opiate receptors, we examined whether [(11)C]dLop, a wea
113 xonium-irreversible, confirming that central opiate receptors were solely responsible for mediating a
114  accumbens have a moderately high density of opiate receptors, which allows for manipulation of opiat

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