ChemInform Abstract: Design and Synthesis of a Metabolically Stable and Potent Antitussive Agent, a Novel δ Opioid Receptor Antagonist, TRK-851.

ChemInform ◽  
2009 ◽  
Vol 40 (6) ◽  
Author(s):  
Hiroshi Nagase ◽  
et al. et al.
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Design And Synthesis ◽  
Opioid Receptor Antagonist ◽  
Δ Opioid Receptor

Design and synthesis of a metabolically stable and potent antitussive agent, a novel δ opioid receptor antagonist, TRK-851

2008 ◽  
Vol 16 (17) ◽  
pp. 7956-7967 ◽  
Author(s):  
Satoshi Sakami ◽  
Koji Kawai ◽  
Masayuki Maeda ◽  
Takumi Aoki ◽  
Hideaki Fujii ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Design And Synthesis ◽  
Opioid Receptor Antagonist ◽  
Δ Opioid Receptor

Behavioral effects of benzylideneoxymorphone (BOM), a low efficacy µ opioid receptor agonist and a δ opioid receptor antagonist

2020 ◽  
Vol 237 (12) ◽  
pp. 3591-3602
Author(s):  
Sanjana Mada ◽  
Lisa R. Gerak ◽  
Amélie Soyer ◽  
David R. Maguire ◽  
Zehua Hu ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Receptor Agonist ◽  
Behavioral Effects ◽  
Opioid Receptor Antagonist ◽  
Opioid Receptor Agonist ◽  
Δ Opioid Receptor

δ-Opioid Receptor Antagonist Inhibits Immunomodulation by Met-Enkephalin Analogs

1999 ◽  
Vol 6 (5) ◽  
pp. 355-360 ◽  
Author(s):  
Vijay K. Singh ◽  
Kirti Bajpai ◽  
Prem Narayan ◽  
Virendra S. Yadav ◽  
Vikas C. Dhawan ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Opioid Receptor Antagonist ◽  
Δ Opioid Receptor

Highly Selective Fluorescent Analogue of the Potent δ-Opioid Receptor Antagonist Dmt-Tic

2004 ◽  
Vol 47 (26) ◽  
pp. 6541-6546 ◽  
Author(s):  
Gianfranco Balboni ◽  
Severo Salvadori ◽  
Alessandro Dal Piaz ◽  
Fabrizio Bortolotti ◽  
Roberto Argazzi ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Opioid Receptor Antagonist ◽  
Δ Opioid Receptor

scholarly journals Interactions of galanin with endomophin-2, vasopressin and oxytocin in nociceptive modulation of the trigemino-hypoglossal reflex in rats

2008 ◽  
pp. 769-776
Author(s):  
M Zubrzycka ◽  
A Janecka
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Antinociceptive Effect ◽  
Tooth Pulp ◽  
Cerebral Ventricles ◽  
Galanin Receptor ◽  
The Third ◽  
Opioid Receptor Antagonist ◽  
Pain Transmission ◽  
Δ Opioid Receptor

Galanin (GAL) is suggested to be a neuropeptide involved in pain transmission. In this study we tried to determine, whether the increase of GAL concentration in brain cells affects impulse transmission between the motor centers localized in the vicinity of the third and fourth cerebral ventricles. The experiments were carried out on rats under chloralose anesthesia. The study objectives were realized using the method allowing to record the amplitude of evoked tongue jerks (ETJ) in response to noxious tooth pulp stimulation during the perfusion of the cerebral ventricles with solutions containing tested compounds. Perfusion of the cerebral ventricles with GAL concentration-dependently inhibited the ETJ amplitude. The antinociceptive effect of GAL was blocked by a galanin receptor antagonist, galantide (GLT) and by opioid antagonists: non-selective naloxone (Nal) and μselective β-funaltrexamine (β-FNA). In contrast, a δ-opioid receptor antagonist, naltrindole (NTI) or the κ-opioid receptor antagonist, nor-binaltrophimine (nor-BNI) did not inhibit the effect of GAL. The antinociceptive effect of GAL was more pronounced when GAL was perfused in combination with other neuropeptides/neurohormones, such as endomorphin-2 (EM-2), vasopressin (AVP) and oxytocin (OT). The present results demonstrate that in the orofacial area analgesic activity is modulated by GAL, OT and AVP and that EM-2-induced antinociception involves GAL.

Synaptic Actions of Neuropeptide FF in the Rat Parabrachial Nucleus: Interactions With Opioid Receptors

2000 ◽  
Vol 84 (2) ◽  
pp. 744-751 ◽  
Author(s):  
Xihua Chen ◽  
Jeffrey A. Zidichouski ◽  
Kim H. Harris ◽  
Jack H. Jhamandas
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Distribution Curve ◽  
Parabrachial Nucleus ◽  
Synaptic Currents ◽  
Opioid Receptor Antagonist ◽  
Neuropeptide Ff ◽  
Δ Opioid Receptor ◽  
Synaptic Effects

The pontine parabrachial nucleus (PBN) receives both opioid and Neuropeptide FF (NPFF) projections from the lower brain stem and/or the spinal cord. Because of this anatomical convergence and previous evidence that NPFF displays both pro- and anti-opioid activities, this study examined the synaptic effects of NPFF in the PBN and the mechanisms underlying these effects using an in vitro brain slice preparation and the nystatin-perforated patch-clamp recording technique. Under voltage-clamp conditions, NPFF reversibly reduced the evoked excitatory postsynaptic currents (EPSCs) in a dose-dependent fashion. This effect was not accompanied by apparent changes in the holding current, the current-voltage relationship or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid–induced inward currents in the PBN cells. When a paired-pulse protocol was used, NPFF increased the ratio of these synaptic currents. Analysis of miniature EPSCs showed that NPFF caused a rightward shift in the frequency-distribution curve, whereas the amplitude-distribution curve remained unchanged. Collectively, these experiments indicate that NPFF reduces the evoked EPSCs through a presynaptic mechanism of action. The synaptic effects induced by NPFF (5 μM) could not be blocked by the specific μ-opioid receptor antagonist,d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2(1 μM), but application of δ-opioid receptor antagonist Tyr-Tic-Phe-Phe (5 μM) almost completely prevented effects of NPFF. Moreover, the δ-opioid receptor agonist, Deltorphin (1 μM), mimicked the effects as NPFF and also occluded NPFF's actions on synaptic currents. These results indicate that NPFF modulates excitatory synaptic transmission in the PBN through an interaction with presynaptic δ-opioid receptors. These observations provide a cellular basis for NPFF enhancement of the antinociceptive effects consequent to central activation of δ-opioid receptors.

scholarly journals Dark chocolate receptors: epicatechin-induced cardiac protection is dependent on δ-opioid receptor stimulation

2010 ◽  
Vol 299 (5) ◽  
pp. H1604-H1609 ◽  
Author(s):  
Mathivadhani Panneerselvam ◽  
Yasuo M. Tsutsumi ◽  
Jacqueline A. Bonds ◽  
Yousuke T. Horikawa ◽  
Michelle Saldana ◽  
...  
Keyword(s):  
Infarct Size ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Low Dose ◽  
Ischemia Reperfusion ◽  
Receptor Activation ◽  
Cardiac Protection ◽  
Receptor Stimulation ◽  
Opioid Receptor Antagonist ◽  
Δ Opioid Receptor

Epicatechin, a flavonoid, is a well-known antioxidant linked to a variety of protective effects in both humans and animals. In particular, its role in protection against cardiovascular disease has been demonstrated by epidemiologic studies. Low-dose epicatechin, which does not have significant antioxidant activity, is also protective; however, the mechanism by which low-dose epicatechin induces this effect is unknown. Our laboratory tested the hypothesis that low-dose epicatechin mediates cardiac protection via opioid receptor activation. C57BL/6 mice were randomly assigned to 1 of 10 groups: control, epicatechin, naloxone (nonselective opioid receptor antagonist), epicatechin + naloxone, naltrindole (δ-specific opioid receptor antagonist), epicatechin + naltrindole, norbinaltorphimine (nor-BNI, κ-specific opioid receptor antagonist), epicatechin + nor-BNI, 5-hydroxydecanoic acid [5-HD, ATP-sensitive potassium channel antagonist], and epicatechin + 5-HD. Epicatechin (1 mg/kg) or other inhibitors (5 mg/kg) were administered by oral gavage or intraperitoneal injection, respectively, daily for 10 days. Mice were subjected to 30 min coronary artery occlusion followed by 2 h of reperfusion, and infarct size was determined via planimetry. Whole heart homogenates were assayed for downstream opioid receptor signaling targets. Infarct size was significantly reduced in epicatechin- and epicatechin + nor-BNI-treated mice compared with control mice. This protection was blocked by naloxone, naltrindole, and 5-HD. Epicatechin and epicatechin + nor-BNI increased the phosphorylation of Src, Akt, and IκBα, while simultaneously decreasing the expression of c-Jun NH2-terminal kinase and caspase-activated DNase. All signaling effects are consistent with opioid receptor stimulation and subsequent cardiac protection. Naloxone, naltrindole, and 5-HD attenuated these effects. In conclusion, epicatechin acts via opioid receptors and more specifically through the δ-opioid receptor to produce cardiac protection from ischemia-reperfusion injury.

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