Relevant bibliographies by topics / Delta-opioid agonists

Academic literature on the topic 'Delta-opioid agonists'

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Published: 4 June 2021
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Journal articles on the topic "Delta-opioid agonists"

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Grider, J. R., and G. M. Makhlouf. "Identification of opioid receptors on gastric muscle cells by selective receptor protection." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 1 (January 1, 1991): G103—G107. http://dx.doi.org/10.1152/ajpgi.1991.260.1.g103.

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Opioid receptors on isolated gastric smooth muscle cells were characterized pharmacologically by a technique in which synthetic selective opioid agonists and antagonists were used to protect and thus enrich a specific receptor type while all other receptors were inactivated by N-ethylamaleimide. Treatment of the cells with the selective mu-receptor agonist DAGO or antagonist CTAP preserved only the response to DAGO; treatment with the selective delta-receptor agonist DPDPE or antagonist naltrindole preserved only the response to DPPE; and treatment with the selective kappa-receptor agonist U50,488H or antagonist nor-binaltorphimine preserved only the response to U50,488H. The results established the presence of distinct kappa-, delta-, and mu-opioid receptors capable of mediating contraction of isolated gastric muscle cells. The pattern of interaction of endogenous opioid peptides with protected receptors implied that dynorphin-(1-13) and Met-enkephalin were selective agonists for kappa- and delta-opioid receptors, respectively, and Leu-enkephalin a preferential agonist of mu-opioid receptors. The results were confirmed by a reverse approach in which opioid receptors were inactivated by site-directed irreversible antagonists. beta-Funaltrexamine, a mu-selective antagonist, abolished the response to mu-receptor agonists, whereas beta-chlornaltrexamine, a mu- and kappa-selective antagonist, abolished the response to mu-receptor agonists and partially inhibited the response to kappa-receptor agonists.
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Loriga, Giovanni, Paolo Lazzari, Ilaria Manca, Stefania Ruiu, Matteo Falzoi, Gabriele Murineddu, Mirko Emilio Heiner Bottazzi, Giovanni Pinna, and Gérard Aimè Pinna. "Novel diazabicycloalkane delta opioid agonists." Bioorganic & Medicinal Chemistry 23, no. 17 (September 2015): 5527–38. http://dx.doi.org/10.1016/j.bmc.2015.07.036.

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Vankova, Miriana E., Matthew B. Weinger, Dong-Yi Chen, J. Brian Bronson, Valerie Motis, and George F. Koob. "Role Central Mu, Delta-1, and Kappa-1 Opioid Receptors in Opioid-induced Muscle Rigidity in the Rat." Anesthesiology 85, no. 3 (September 1, 1996): 574–83. http://dx.doi.org/10.1097/00000542-199609000-00017.

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Background Opioids appear to produce their physiologic effects by binding to at least three types of opioid receptors, the mu (mu), delta (delta), and kappa (kappa) receptors. Muscle rigidity occurs after administration of supra-analgesic doses of potent mu-preferring agonists like alfentanil. The role of different supraspinal opioid receptors in this rigidity has been addressed only recently. To elucidate the contribution of central mu, delta, and kappa receptors to muscle rigidity, the effects of intracerebroventricularly administered opioid receptor-selective agonists and antagonists on alfentanil-induced muscle rigidity were examined in rats. Methods Rats in which chronic intracerebroventricular cannulae had been implanted received an intracerebroventricular infusion of either saline or a mu (D-Ala2,N-Me-Phe4-Gly5-olenkephalin; DAMGO), delta(1) (D-Pen2,D-Pen5-enkephalin; DPDPE), or kappa(1) (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)- cyclohexyl)-benzene-acetamide methane sulfonate; U50,488H) opioid agonist. Ten minutes later, they received either saline or the mu-agonist alfentanil subcutaneously. Muscle rigidity was assessed using hindlimb electromyographic activity. Different groups of animals were pretreated with an intracerebroventricular infusion of either saline or a mu (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2; CTAP), delta (naltrindole), or kappa(1) (norbinaltorphimine) opioid antagonist before administration of either saline or a selective intracerebroventricular agonist. Results The mu agonist DAMGO alone dose-dependently induced muscle rigidity. This effect was antagonized by pretreatment with the mu-selective antagonist CTAP. Neither DPDPE nor U50,488H, when administered alone, affected muscle tone. However, both the delta(1) and kappa(1) agonists dose-dependently attenuated alfentanil-induced rigidity. This antagonism of alfentanil rigidity was abolished after pretreatment with the delta (naltrindole) and kappa(1) (nor-binaltorphimine) antagonists, respectively. Conclusions The present data demonstrate that whereas systemic opiate-induced muscle rigidity is primarily due to the activation of central mu receptors, supraspinal delta(1) and kappa(1) receptors may attenuate this effect. This finding is consistent with previous demonstrations of functional interactions between different central opioid receptor populations in other opiate effects, and could have important pharmacotherapeutic implications.
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Haddad, G. G., H. J. Jeng, and T. L. Lai. "Effect of endorphins on heart rate and blood pressure in adult dogs." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 5 (May 1, 1986): H796—H805. http://dx.doi.org/10.1152/ajpheart.1986.250.5.h796.

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To investigate the role of opioids in regulating cardiovascular function, we administered delta-opioid receptor agonists D-Ala-D-Leu enkephalin (DADLE) and D-Ala-Met enkephalinamide (DAME), and mu-opioid receptor agonist, a morphiceptin analogue (MA), intracisternally in 13 unanesthetized, chronically instrumented adult dogs in 2 doses (25 and 125 micrograms/kg). After an initial transient drop, the R-R interval increased (peak approximately 25–60 min) postadministration of opioids. The time course and the magnitude of the change in R-R interval depended on the agonist: delta-agonists induced a more prolonged and marked change in R-R interval than mu-agonists at both doses. Mean arterial blood pressure (MAP) increased initially but dropped toward or even below base line 30 min after opioids administration. Atropine, given intravenously or intra-arterially at peak action of agonist in relatively low doses (0.02 mg/kg), induced an AV block followed by a marked decrease in R-R interval. There was also an increase in MAP after atropine. Naloxone, given intracisternally, reversed both delta- and mu-opioid effects but did not induce changes in the R-R interval without prior administration of opioids. We conclude that in unanesthetized adult dogs 1) both mu- and delta-receptor opioid agonists prolong the R-R interval, and this depends on the type of receptor stimulated; 2) opioids induce slowing in heart rate, possibly by increasing parasympathetic activity to the heart; 3) enkephalin and morphiceptin analogues induce a biphasic response in MAP; and 4) endorphins do not modulate cardiovascular function tonically; we speculate that they can alter the R-R interval and MAP in the presence of stimuli.
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Negus, S. Stevens, Ember M. Morrissey, John E. Folk, and Kenner C. Rice. "Interaction between Mu and Delta Opioid Receptor Agonists in an Assay of Capsaicin-Induced Thermal Allodynia in Rhesus Monkeys." Pain Research and Treatment 2012 (May 14, 2012): 1–8. http://dx.doi.org/10.1155/2012/867067.

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Delta opioid agonists enhance antinociceptive effects of mu-opioid agonists in many preclinical assays of acute nociception, but delta/mu interactions in preclinical models of inflammation-associated pain have not been examined. This study examined interactions between the delta agonist SNC80 [(+)-4-[(αR)-α-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide] and the mu agonist analgesics methadone, morphine, and nalbuphine in an assay of capsaicin-induced thermal allodynia in rhesus monkeys. Thermal allodynia was produced by topical application of capsaicin to the tail. Antiallodynic effects of methadone, morphine, and nalbuphine were evaluated alone or in combination with fixed proportions of SNC80 identical to proportions previously shown to enhance acute thermal antinociceptive effects of these mu agonists in rhesus monkeys (0.9 : 1 SNC80/methadone; 0.29 : 1 SNC80/morphine; 3.6 : 1 SNC80/nalbuphine). Methadone, morphine, and nalbuphine each produced dose-dependent antiallodynia. SNC80 produced partial antiallodynia up to the highest dose tested (5.6 mg/kg). SNC80 produced a modest, enantioselective, and naltrindole-reversible enhancement of methadone-induced antiallodynia. However, SNC80 did not enhance morphine antiallodynia and only weakly enhanced nalbuphine antiallodynia. Overall, SNC80 produced modest or no enhancement of the antiallodynic effects of the three mu agonists evaluated. These results suggest that delta agonist-induced enhancement of mu agonist antiallodynia may be weaker and less reliable than previously demonstrated enhancement of mu agonist acute thermal nociception.
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Zhang, L., Z. F. Gu, T. Pradhan, R. T. Jensen, and P. N. Maton. "Characterization of opioid receptors on smooth muscle cells from guinea pig stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 3 (March 1, 1992): G461—G469. http://dx.doi.org/10.1152/ajpgi.1992.262.3.g461.

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On the basis of opioid-stimulated contraction of dispersed gastric smooth muscle cells it has been suggested that these cells possess opioid receptors of three subtypes: kappa (kappa), mu (mu), and delta (delta). We have used selective peptidase-resistant radioligands, agonists and antagonists, to examine receptor subtypes on dispersed gastric smooth muscle cells from guinea pigs prepared by collagenase digestion. The kappa-agonist U-50488H, the mu-agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO), and the delta-agonist [D-Pen2,Pen5]enkephalin (DPDPE) each caused muscle contraction. The concentrations required to caused half-maximal contraction were U50488H (6 pM) greater than DAGO (13 pM) greater than DPDPE (6 nM). The abilities of these agonists to inhibit binding of [3H]U-69593 (kappa-preferring) by 50% were U50488H (43 nM) greater than DAGO (43 microM) greater than DPDPE (200 microM). Their abilities to inhibit binding of [3H]naloxone (mu-preferring) by 50% were DAGO (0.2 microM) greater than U50488H (10 microM) greater than DPDPE (greater than 100 microM). No binding could be detected with the delta-selective ligand [3H]DPDPE. The kappa-preferring antagonist Mr2266 (10 nM) preferentially inhibited contraction stimulated by the kappa-agonist U50488H, and naltrexone (10 nM) (mu-selective antagonist) preferentially inhibited contraction stimulated by the mu-agonist DAGO. ICI 174864 (200 microM; delta-selective antagonist) had no effect on contraction stimulated by mu-, kappa-, or delta-agonists. Contraction stimulated by the delta-agonist DPDPE was inhibited by both kappa- and mu-receptor antagonists. Studies on the effect of the antagonists on binding of [3H]naloxone and [3H]U69593 also provided evidence for kappa- and mu-sites but nor for delta-sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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Schaeffer, J. I., and G. G. Haddad. "Regulation of ventilation and oxygen consumption by delta- and mu-opioid receptor agonists." Journal of Applied Physiology 59, no. 3 (September 1, 1985): 959–68. http://dx.doi.org/10.1152/jappl.1985.59.3.959.

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To study the effect of endorphins on metabolic rate and on the relationship between O2 consumption (VO2) and ventilation, we administered enkephalin analogues (relatively selective delta-receptor agonists) and a morphiceptin analogue (a highly selective mu-receptor agonist) intracisternally in nine unanesthetized chronically instrumented adult dogs. Both delta- and mu-agonists decreased VO2 by 40–60%. delta-Agonists induced a dose-dependent decrease in mean instantaneous minute ventilation (VT/TT) associated with periodic breathing. The decrease in VT/TT started and resolved prior to the decrease and returned to baseline of VO2, respectively. In contrast, the mu-agonists induced an increase in VT/TT associated with rapid shallow breathing. Arterial PCO2 increased and arterial PO2 decreased after both delta- and mu-agonists. Low doses of intracisternal naloxone (0.002–2.0 micrograms/kg) reversed the opioid effect on VT/TT but not on VO2; higher doses of naloxone (5–25 micrograms/kg) reversed both. Naloxone administered alone had no effect on VT/TT or VO2. These data suggest that 1) both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, 2) this hypoventilation results from a decrease in VT/TT after delta-agonists but an increase in dead space ventilation after mu-agonists, and 3) endorphins do not modulate ventilation and metabolic rate tonically, but we speculate that they may do so in response to stressful stimulation.
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Kumar, V., M. J. Clark, J. R. Traynor, J. W. Lewis, and S. M. Husbands. "Pyrrolo- and pyridomorphinans: Non-selective opioid antagonists and delta opioid agonists/mu opioid partial agonists." Bioorganic & Medicinal Chemistry 22, no. 15 (August 2014): 4067–72. http://dx.doi.org/10.1016/j.bmc.2014.05.065.

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Pham, Thao, Louis Carrega, Nicole Sauze, Odile Fund-Saunier, Christiane Devaux, Jean-Claude Peragut, Alain Saadjian, and Régis Guieu. "Supraspinal Antinociceptive Effects of μ and δ Agonists Involve Modulation of Adenosine Uptake." Anesthesiology 98, no. 2 (February 1, 2003): 459–64. http://dx.doi.org/10.1097/00000542-200302000-00027.

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Background The modulation of extracellular adenosine concentration by opioids provides evidence that the antinociceptive effects of these compounds involve endogenous adenosine. The aim of this study was to determine whether there is a relation between the inhibition of brain synaptosome adenosine uptake by opioid agonists and the analgesic effects of these compounds. Methods The authors used the hot plate and tail-pinch tests to evaluate in mice (C57BL/6 females; weight, 25-30 g) the effects of caffeine, a nonspecific adenosine receptor antagonist, on the antinociceptive effect induced by the intracerebroventricular administration of oxymorphone as a mu agonist, SNC80 as a delta agonist, or U69593 as a kappa agonist. They also investigated the effect of these opioid receptor agonists on the uptake of adenosine by whole brain synaptosomes. Results Caffeine decreased the analgesic effects induced by oxymorphone or SNC80 but not those induced by U69593. Oxymorphone and SNC80 inhibited adenosine uptake by brain cells, but U69593 did not. Conclusion The antinociceptive effects obtained with mu or delta (but not kappa) agonists administered supraspinally were indicative of the involvement of modulation of adenosine uptake.
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Ikoma, Miho, Tatsuro Kohno, and Hiroshi Baba. "Differential Presynaptic Effects of Opioid Agonists on Aδ- and C-afferent Glutamatergic Transmission to the Spinal Dorsal Horn." Anesthesiology 107, no. 5 (November 1, 2007): 807–12. http://dx.doi.org/10.1097/01.anes.0000286985.80301.5e.

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Background Although intrathecal administration of opioids produces antinociceptive effects in the spinal cord, it has not been established whether intrathecal opioid application more effectively terminates C fiber-mediated pain than A fiber-mediated pain. Here, the authors focus on the differences in opioid actions on Adelta- and C-afferent responses. Methods Using the whole cell patch clamp technique, the authors investigated the presynaptic inhibitory actions of micro-, delta-, and kappa-opioid receptor agonists on primary afferent-evoked excitatory postsynaptic currents (EPSCs) in substantia gelatinosa neurons of adult rat spinal cord slices. Results The micro agonist DAMGO (0.1, 1 microM) reduced the amplitude of glutamatergic monosynaptic Adelta- or C fiber-evoked EPSCs. C fiber-evoked EPSCs were inhibited to a greater extent than Adelta fiber-evoked EPSCs. The delta agonist DPDPE (1, 10 microM) produced modest inhibition of Adelta- or C fiber-evoked EPSCs. In contrast, the kappa agonist U69593 (1 microM) did not affect the amplitude of either Adelta or C fiber-evoked EPSCs. Conclusions These results indicate that opioids suppress excitatory synaptic transmission mainly through activation of micro receptors on primary afferent C fibers. Given that the substantia gelatinosa is the main termination of Adelta and C fibers transmitting nociceptive information, the current findings may partially explain the different potency of opioid agonists.
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Dissertations / Theses on the topic "Delta-opioid agonists"

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Asghar, Muhammad Junaid. "Studies on the biased signalling of some novel delta opioid receptor agonists." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40485/.

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The delta opioid receptor (DOR) is a G protein-coupled receptor (GPCR) which is important in the regulation of neuronal function, predominantly via coupling to heterotrimeric Gi/0 proteins. The receptor has been shown to be a potential target for the treatment of chronic pain and affective disorders. Although a large number of opioid agonists exist, their properties vary widely, at least partly due to their differential coupling to post-receptor signalling systems, a phenomenon referred to as ligand-biased signalling or functional selectivity. The aim of the current project was to examine the signalling properties of a set of established and novel DOR agonists in an attempt to identify compounds that have biased signalling profiles. It was hypothesized that DOR agonists with partial efficacy regarding β-arrestin recruitment would be less liable to induce receptor internalization and desensitization of G protein-mediated signalling than full agonists. Chinese hamster ovary (CHO) cells, stably transfected with GFP-tagged human (h)DOR and CHO-K1 and U2OS cells over-expressing hDOR were exposed to a number of novel selective DOR agonists compared with the commercially available agonists, SNC80, ADL5859 and DADLE. The compounds’ potencies and efficacies were measured in four different assay systems; 1. Inhibition of forskolin-stimulated cyclic AMP accumulation, 2. Extracellular signal-regulated kinase (ERK1/2) phosphorylation using an immunocytochemical In-cell Western (I-CW) assay, 3. β-arrestin 2 recruitment and 4. hDOR internalization. The latter two assays employed DiscoverX Enzyme Fragment Complementation technology. An attempt to develop a secreted placental alkaline phosphatase (SPAP) reporter gene assay to measure DOR-mediated cyclic AMP inhibition was not successful. All of the ligands were nearly full agonists in relation to cyclic AMP inhibition although some were less efficacious than the standard SNC80 regarding ERK1/2 activation. Their absolute potencies and rank orders of potency in inhibiting cyclic AMP and activating ERK1/2 were quite different, although both signalling systems were apparently Gi/o- protein mediated. In contrast, the agonists exhibited a full range of efficacies and potencies in both β-arrestin 2 recruitment and hDOR internalization assays and there was a significant correlation between the maximum efficacies of the compounds in the two assays. A potential relationship between β-arrestin 2 recruitment/ hDOR internalization and desensitization of agonist-induced cyclic AMP accumulation was explored. Responses to the highly arrestin-recruiting agonists SNC80 and DADLE desensitized fully after extended exposure, whereas the novel partial agonists PN6047 and OPD00003 resisted desensitization. Bias factors were calculated for the agonist set and both PN6047 and OPD00003 were found to be significantly biased towards G protein-mediated cyclic AMP inhibition. In conclusion, this study reports, for the first time, a detailed characterization of signalling bias for a set of selective DOR agonists in cells over-expressing human DORs. The findings suggest that it is potentially possible to predict wanted and unwanted properties of agonists by determining post-receptor signalling profiles in vitro which will facilitate the discovery and development of novel therapeutics based on the DOR.
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Vanderah, Todd William. "The direct and modulatory antinociceptive actions of endogenous and exogenous opioid delta agonists." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187190.

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Opioids are responsible for a number of effects but are employed primarily as analgesics. The discovery of endogenous opioids and multiple receptors have led to a better understanding of how analgesics function, and how both opioid receptors and endogenous ligands are regulated. The hypothesis of this dissertation states that levels of endogenous enkephalins are modulated by stress, inflammation and the endogenous peptide cholecystokinin (CCK) to alter the antinociceptive efficacy of μ and, possibly, δ opioids. Endogenous enkephalin release results in either direct antinociception or synergistically enhances the antinociceptive effects of the μ agonist morphine via δ receptors. This thesis will first detail how the administration of exogenous δ compounds can enhance the antinociceptive effects of a μ agonist. Exposure of mice to a cold-water swim-stress (CWSS) paradigm resulted in direct antinociception that was attenuated by opioid antagonists. Exposure to CWSS for a limited amount of time did not produce significant antinociception, but produced a marked enhancement of morphine antinociception. This enhancement was blocked by the administration of δ antagonists and (Leu⁵) enkephalin antisera. An antisense oligodeoxynucleotide was designed from the δ opioid receptor and administered to animals. Animals treated with the δ antisense and exposed to the CWSS paradigm showed a significant decrease in antinociception. Inflammation produced in the hind-paw of the mouse significantly enhanced the antinociceptive effects of morphine that was inhibited by δ antagonists and (Leu⁵) enkephalin antisera. The administration of a selective CCK(B) antagonist, L365,260 or CCK(B) antisense, enhances the antinociceptive potency of morphine. This enhancement is attenuated by δ antagonists, (Leu⁵) enkephalin antisera, as well as exhibits a two-way cross tolerance with δ agonists. L365,260 and an "enkephalinase" inhibitor, when coadministered, produced significant antinociception that was blocked by a δ antagonist and (Leu⁵) enkephalin antisera. Using polymerase chain reaction in search of a δ opioid receptor subtype, an orphan receptor was cloned and characterized as a member of the G protein-coupled receptor family. These data suggest that stress results in the release of (Leu⁵) enkephalin that enhances the antinociceptive effects of a μ-selective agonist morphine. Release of endogenous enkephalins may be regulated by the interactions of cholecystokinin at the CCK(B)receptor. Such information may lead to appropriate use of opiates in conjunction with CCK antagonists for the management of appropriate pain states.
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Moon, Hyo-Eun. "Differential G protein activation by fusion proteins between the human #delta#-opioid receptor and G←i₁α/G←o₁α proteins." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366183.

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Qian, Xinhua. "Topographical design of the message domain pharmacophore of the delta opioid agonists using designer amino acids and design of non-peptide ligand for opioid receptors." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187062.

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A series of highly constrained tyrosine derivatives, 2',6'-dimethyl- β-methyltyrosines (TMTs), was designed and asymmetrically synthesized. Incorporation of the TMT isomers into peptide agonists of δ opioid receptors provide analogues that are highly potent and selectively for δ opioid receptors and have revealed the stereochemical requirements for recognizing opioid δ receptors. Moreover, the combination of conformational studies and pharmacological studies of the peptide analogues provided for the first time the stereochemical requirements for specifically recognizing opioid δ receptor subtypes. The biological active conformation of a highly selective and potent δ opioid agonist, ((2S,3R)-TMT¹) DPDPE, was obtained by NMR studies and computer-assisted modeling. This conformation was then further used for designing novel non-peptide opioid ligands. Thus, this study is another achievement of topographical design of peptide hormones and neurotransmitters. Practically, the results of this study can be used to develop more biological stable pharmaceuticals as strong pain reliever without causing side effects such as physical dependence, respiratory depression, etc.
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Nickel, Frank. "Über die kardioprotektive Wirkung eines d-Opioid-Agonisten [Delta-Opioid-Agonisten] auf das ischämisch-reperfundierte Myokard in Abhängigkeit von freien Radikalen eine Studie an blutperfundierten, isolierten Kaninchenherzen /." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966043758.

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Wrigley, Paul John. "Cold thermal processing in the spinal cord." 2006. http://hdl.handle.net/2123/1619.

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Doctor of Philosophy(PhD)
Two recently identified transient receptor potential (TRP) channels, TRPM8 and TRPA1, have been proposed to play an important role in mammalian cool and cold peripheral sensory transduction. When expressed in cell-lines the cloned TRPM8 and TRPA1 receptors have distinct pharmacological and temperature response characteristics. Although these receptors are also transported to the central terminals of primary afferents, little is known about their centrally mediated actions. In this thesis, I use an in vitro electrophysiological approach to investigate the dorsal horn processing of cool afferent modalities and the role of TRP ion channels. The results of this thesis provide further information on thermal processing, indicate direction for further research and suggest possible therapeutic targets for the management of abnormal cold sensory processing. Initial experiments demonstrate that the cooling agents and known TRPM8 and TRPA1 agonists, menthol and icilin, inhibit primary afferent evoked excitatory postsynaptic currents (EPSCs) in rat spinal cord dorsal horn neurons. In addition, temperature reduction, menthol and icilin increase the frequency of miniature EPSCs without affecting amplitude distribution or kinetics. Little or no direct postsynaptic effect on dorsal horn neurons, GABAergic or glycinergic transmission was found. In combination, these observations demonstrate that temperature reduction, menthol and icilin act presynaptically to increase the probability of glutamate release from primary afferent fibres. Further examination of the changes in glutamatergic synaptic transmission induced by temperature reduction, menthol and icilin reveals a subset of neurons sensitive to innocuous cool (< 29 oC) and low concentrations of icilin (3-10 µM) which closely match the temperature activation and pharmacological profile of TRPM8. In addition, the majority of lamina I and II neurons displayed characteristics partly consistent with TRPA1-activation, including a concentration-dependent response to icilin and blockade by ruthenium red. The present experiments did not allow thermal characterisation of these TRPA1-like responses. Together these observations indicate that the effects of menthol and icilin on glutamatergic synaptic transmission in the superficial dorsal horn are mediated by TRPM8 and possibly by TRPA1. Examination of the anatomical location of neurons activated by temperature reduction, menthol, icilin and capsaicin allowed the central termination pattern of thermoreceptive primary afferent fibres with specific TRP-like response characteristics to be determined. TRPM8-like presynaptic activation was confined to a subpopulation of neurons located in lamina I and outer lamina II, while the majority of neurons throughout laminae I and II received inputs sensitive to menthol, high concentrations of icilin and capsaicin. These findings suggest that innocuous cool sensation projects to a specific subpopulation of superficial dorsal horn neurons unlike other modalities (mediated by TRPV1, possibly TRPA1 and other receptors), which non-selectively engage circuits within the entire superficial dorsal horn. No morphological specificity was identified for recovered neurons after electrophysiological characterisation. Finally, mu-opioids were shown to inhibit basal glutamatergic synaptic transmission as well as menthol- and icilin-induced transmission in the superficial dorsal horn. Of particular interest, delta-opioids selectively inhibited icilin-induced synaptic transmission within the same location. The selective effect of delta-opioids suggests a possible role in modulating receptors activated by icilin (TRPM8 and TRPA1). Overall, this thesis provides further evidence that TRPM8 is responsible for the transduction of innocuous cold sensation in mammals and is a potential therapeutic target in humans with cold hyperaesthesia secondary to abnormal thermal processing. The use of delta-opioid agonists warrants further investigation in cold hypersensitivity states and potentially other forms of pain.
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Nickel, Frank [Verfasser]. "Über die kardioprotektive Wirkung eines δ-Opioid-Agonisten [Delta-Opioid-Agonisten] auf das ischämisch-reperfundierte Myokard in Abhängigkeit von freien Radikalen : eine Studie an blutperfundierten, isolierten Kaninchenherzen / vorgelegt von Frank Nickel." 2002. http://d-nb.info/966043758/34.

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Wolfrum, Elmar [Verfasser]. "Untersuchungen zur myokardialen Kontraktilität : protektive Wirkung des Delta-Opioid-Rezeptor-Agonisten DADLE im Vergleich zu Bretschneider-Kardioplegie / Elmar Wolfrum." 2009. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-73443.

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WANG, Y. C., and 王奕棋. "Action Mechanisms Involved in the Effect of Non-peptide Opioid Delta-receptor Agonist and Antagonist on the Micturition Reflex in the Rat." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/98791048854741950130.

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碩士
國立臺灣大學
生理學研究所
88
Morphine and a number of other opioid analgesics produce urinary retention in clinical use. This action appears to involve the activation of delta and mu opioid receptors in both supraspinal and spinal levels. Thus, Pharmacologic manipulation of endogenous opioid mechanisms may be clinically useful in treating neurogenic bladder dysfunction, such as urinary incontinence. The purpose of this study is to investigate the action mechanisms of two non-peptide opioid delta-receptor-selective agonists (SNC-80, BW373U86) and an antagonist (naltrindole) involved in the micturition reflex. They were tested by the spontaneous volume-induced contraction of the urinary bladder in the urethane-anesthetized rats. The intravesical pressure, the pelvic afferent activity (PANA) and efferent activities (PENA) as well as the EMG of external urethral sphincter (EUS-EMG) were recorded simultaneously. The intracerebroventricular administration of SNC-80 or BW373U86 caused inhibition of the micturition reflex, and BW373U86 also induced a reduction in peak micturition pressure (PMP) and EUS-EMG. The intrathecal infusion of SNC-80 or BW373U86 produced a complete short-lasting inhibition of micturition reflex. The inhibition of the EUS-EMG, PANA and PENA were persisted when the micturition reappeared. On the other hand, the intracerebroventricular administration of naltrindole, the micturition reflex was facilitated but the PMP was inhibited. Whereas intrathecal infusion of naltrindole produced a series of ineffective bladder contractions before the first micturition started. In local application of SNC-80 or BW373U86, however, the micturition interval, PMP, EUS-EMG, PANA, and PENA were all inhibited. Local application of naltrindole produced the effects just opposite to the agonist stated above, except the PMP, which was reduced in a high dose. The opioid delta receptor agonists and antagonist at the supraspinal site failed to alter the pelvic nerve activity suggest that supraspinal endogenous opioid system does not act directly on the sacral preganglionic neurons, but indirectly through descending fibers on the interneuron at the level of afferent inputs in the sacral spinal cord. However, these agonists at the spinal site may cause direct inhibition of the sacral preganglionic neuron discharge, and then inhibit the pelvic nerve activity. These results indicate that the brain endogenous opioid system seems to play a major role in the modulation of the micturition threshold and the frequency, whereas in the spinal region, enkephalinergic neurons seem to control the activity of sacral preganglionic neurons. It is concluded that the opioid d-receptor agonist, SNC-80, but not BW373U86, may be a good candidate for the treatment of the patient with urinary incontinence.
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Charfi, Iness. "Étude du trafic du récepteur delta-opiacé suite à sa stimulation par différents agonistes." Thèse, 2012. http://hdl.handle.net/1866/8899.

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Les opiacés figurent parmi les analgésiques les plus puissants pour le traitement des douleurs sévères. Les agonistes du DOR (récepteur delta opiacé) induisent moins d'effets secondaires que ceux du mu, ce qui les rend une cible d'intérêt pour le traitement des douleurs chroniques. Cependant, ils induisent la tolérance à l'analgésie. Des hypothèses récentes proposent que le potentiel des drogues à induire la tolérance soit la conséquence de la stabilisation de différentes conformations du récepteur induites par la liaison avec différents ligands, chacune ayant différentes propriétés de trafic. Dans ce contexte, nous avons déterminé si différents ligands du DOR différaient dans leur capacité à induire la signalisation et le trafic du récepteur. Nos résultats indiquent que DPDPE et SNC-80 sont les drogues les plus efficaces à inhiber la production d’AMPc, suivis par UFP-512, morphine et TIPP. DPDPE et SNC-80 induisent à eux seuls l’internalisation du DOR dans les cellules HEK-293 de façon dépendante de la β-arrestine mais pas de la GRK2 ni PKC. Ces deux drogues induisent également l’internalisation du DOR dans les neurones corticaux et c’est seulement le DPDPE qui permet au DOR de regagner la membrane des cellules HEK-293 et des neurones après récupération. Cette capacité de recyclage était suggérée comme un mécanisme protégeant contre la survenue de la tolérance. Ces observations indiquent que le DOR peut subir différentes régulations en fonction du ligand lui étant associé. Cette propriété de sélectivité fonctionnelle des ligands pourrait être utile pour le développement de nouveaux opiacés ayant une activité analgésique plus durable.
Opiates are among the most powerful painkillers to treat severe pain. Delta opioid receptor (DOR) agonists induce fewer side effects than mu opioid receptor agonists, which makes them a target of interest for the treatment of chronic pain. However, they induce tolerance to analgesia. Recent hypotheses suggest that drugs tolerance is the result of stabilization of ligand-specific conformations of the receptor, with distinct traffic properties such as internalization and/or recycling. In this context, we determined whether different DOR ligands differed with respect to their ability to induce signaling and receptor trafficking. Our results indicate that DPDPE and SNC-80 are the most effective drugs to inhibit the production of cAMP, followed by UFP-512, morphine and TIPP. Only DPDPE and SNC-80 manage to induce DOR internalization in HEK-293 cells. This effect is dependent on β-arrestin but not on GRK2 or PKC. Of these two internalizing agonists, only DPDPE allows the DOR to recycle back to the membrane of HEK-293 cells after recovery. DPDPE and SNC-80 also trigger similar DOR internalization in cortical neurons, and as observed in HEK293 cells only DPDPE allowed the receptor to recycle back to the membrane. This recycling capacity was suggested as a mechanism to protect against the onset of tolerance. These observations indicate that the DOR can undergo different regulations depending on the ligand bound to it. This property of functional selectivity of DOR ligands could be useful for the development of new opiates with longer lasting analgesic properties.
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Book chapters on the topic "Delta-opioid agonists"

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Shahabi, N. A., and B. M. Sharp. "Delta Opioid Agonists Inhibit Proliferation of Highlypurified Murine CD4+ and CD8+ T-Cells." In The Brain Immune Axis and Substance Abuse, 29–36. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1951-5_5.

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Calderon, Silvia N. "Nonpeptidic Delta (δ) Opioid Agonists and Antagonists of the Diarylmethylpiperazine Class: What Have We Learned?" In Topics in Current Chemistry, 121–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/128_2010_83.

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Medvedev, O. S., E. R. Martynova, and A. M. Hoque. "Effects of Mu- and Delta-Opiate Receptor Agonists on Systemic and Regional Hemodynamics in Conscious Rats." In Opioid Peptides and Blood Pressure Control, 159–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73429-8_17.

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Negus, S. Stevens, and Ahmad A. Altarifi. "Mu, Delta and Kappa Opioid Agonist Effects In Novel Assays of Pain-Depressed Behavior." In ACS Symposium Series, 163–76. Washington, DC: American Chemical Society, 2013. http://dx.doi.org/10.1021/bk-2013-1131.ch009.

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"Opioid Peptide-Derived Delta Antagonists, Inverse Agonists, and Mixed Mu Agonists/Delta Antagonists." In The Delta Receptor, 209–28. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765-15.

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"Antidepressant-like Effects of Delta Opioid Receptor Agonists." In The Delta Receptor, 373–90. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765-23.

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Jutkiewicz, Emily, and James Woods. "Antidepressant-like Effects of Delta Opioid Receptor Agonists." In The Delta Receptor. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765.ch20.

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Schiller, Peter. "Opioid Peptide-Derived Delta Antagonists, Inverse Delta Agonists, and Mixed Mu Agonist/Delta Antagonists." In The Delta Receptor. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765.ch12.

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"Inverse Agonism at the Delta Opioid Receptors." In The Delta Receptor, 229–48. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765-16.

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Varga, Eva, Keiko Hosohata, Yoshiaki Hosohata, Jennifer Tsang, Thomas Burkey, Josue Alfaro-Lopez, Xuejun Tang, Victor Hruby, William Roeske, and Henry Yamamura. "Inverse Agonism at the Delta Opioid Receptors." In The Delta Receptor. CRC Press, 2003. http://dx.doi.org/10.1201/9780203025765.ch13.

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Conference papers on the topic "Delta-opioid agonists"

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Turnaturi, Rita, Carmela Parenti, Girolamo Calò, Santina Chiechio, Agostino Marrazzo, and Lorella Pasquinucci. "From LP2 to 2S-LP2: discovery of a biased dual-target mu/delta opioid receptor agonist for pain management." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07383.

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