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Chemical Compound Review

DAMGE     (2S)-2-[2-[[(2R)-2-[[(2S)-2- amino-3-(4...

Synonyms: DAMGO, Dagol, DAGO, RX 783006, Tyr-ala-gly-(nme)phe-gly-ol, ...
 
 
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Disease relevance of DAMGE

  • Addition of Go, purified from bovine brain, to membranes from pertussis toxin-treated SH-SY5Y cells restored the inhibition of adenylyl cyclase by DAMGO to 70% of that in toxin-untreated cells [1].
  • The opioid antagonist naloxone, which had no effect on paw-withdrawal threshold in normal paws, produced withdrawal threshold in normal paws, produced withdrawal hyperalgesia in DAMGO-tolerant paws [2].
  • DTLET but not, however, DAGO produced a similar effect on homogenates from the adult rat striatum and on membranes from the neuroblastoma x glioma hybrid cell line NG 108-15, two preparations known to possess only delta receptors negatively coupled to adenylate cyclase [3].
  • When MOR1TAG was stably expressed in both neuroblastoma neuro2A and human embryonic kidney HEK293 cells, the opioid agonist [D-Ala2,MePhe4, Gly5-ol]enkephalin (DAMGO) induced a time- and concentration-dependent phosphorylation of the receptor, in both cell lines, that could be reversed by the antagonist naloxone [4].
  • Because of the proposed relationship between opioid abuse and HIV-1 infection, we also examined the impact of DAMGO on chemokine expression in HIV-infected cells [5].
 

Psychiatry related information on DAMGE

  • Intra-VTA DAMGO significantly increased locomotor activity in stressed rats compared to handled control rats [6].
  • Endogenous morphine immunoneutralization decreased thermal response latency and attenuated the anti-nociceptive effect of the mu selective agonist DAMGO in hot plate test suggesting that endogenous morphine is involved in pain modulation [7].
  • Kelatorphan, a potent enkephalinases inhibitor, and opioid receptor agonists DAGO and DTLET, differentially modulate self-stimulation behaviour depending on the site of administration [8].
  • In contrast to the DAMGO-induced selective enhancement of fat intake, food deprivation significantly increased the intake of both diets to the same extent; however, in this case, only the stimulated fat intake was blocked by systemic naltrexone [9].
  • The biochemical status of human brain mu-opioid receptors and alpha 2-adrenoceptors during opiate dependence was studied by means of the binding of [3H] [D-Ala2, MePhe4, Gly-ol5] enkephalin (DAGO) and [3H]clonidine, respectively, in postmortem brains of heroin addicts who had died by opiate overdose or other causes [10].
 

High impact information on DAMGE

  • We examined the effects of the GABAB receptor agonist baclofen and the mu opioid receptor agonist DAGO on postsynaptic currents evoked by minimal stimulation of inhibitory fibers (meIPSCs) in area CA3 [11].
  • Intracellularly applied protein kinase C (PKC) mimics the effect of DAGO, and a specific PKC inhibitor interrupts the sustained potentiation produced by DAGO [12].
  • Transfection of the teleost cDNA into HEK 293 cells resulted in the appearance of a receptor having high affinity for the mu-selective agonist [D-Ala2, MePhe4-Gly-ol5]enkephalin (DAMGO) (Kd = 0.63 +/- 0.15 nM) and for the nonselective antagonist naloxone (Kd = 3.1 +/- 1.3 nM) [13].
  • Moreover, the Anti-R IgG inhibits the specific binding of radiolabeled Tyr-D-Ala-Gly-N-methyl-Phe-Gly-ol (DAMGO; mu-agonist), DSLET (delta-agonist), and naloxone to homogenates of rat brain membranes with equal potency [14].
  • This study focuses on the in vitro influences of morphine and DAMGE (Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol), mu-selective agonists, and U50,488H and U69,593, kappa-selective agonists, on the generation of antibody to sheep erythrocytes in vitro [15].
 

Chemical compound and disease context of DAMGE

 

Biological context of DAMGE

  • In this study, microinjections of the mu-opioid agonist [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO; 1.6 microM) bilaterally into the LC caused a significant impairment in the development of a heart-rate (HR) conditioned response (CR) [21].
  • Specific agonists for NK-1, NK-2, and NK-3 and delta opioid receptors, carboxyterminal fragments of SP, and a variety of other peptides did not compete at the 3H-SP(1-7) binding sites, but structurally related N-terminal peptides and (D-Ala2, NMe-Phe4, Gly-ol)-enkephalin (DAMGO) were active in displacing the ligand [22].
  • Superfusion of DAMGO did not alter membrane potential, input resistance, or the inward relaxations [23].
  • At concentrations that reduced evoked EPSP/EPSCs by 40-60%, neither DAMGO, DPDPE, nor DELT decreased the amplitude of the postsynaptic current produced by brief pressure ejection of (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, suggesting a presynaptic site of action of these opioid receptor agonists [24].
  • These results indicate a complex DAMGO modulation of the NMDA component of glutamatergic synaptic transmission in NAcc: mu receptor activation decreases NMDA-EPSP amplitudes presynaptically yet increases NMDA currents postsynaptically [23].
 

Anatomical context of DAMGE

 

Associations of DAMGE with other chemical compounds

  • Competition experiments with [3H]DAMGE and [3H]DTLET on crude rat brain membranes showed that the azido photoprobes display a similar (AZ-DAMGE) and even a better (AZ-DTLET) selectivity than their respective parent compounds DAMGE and DTLET [29].
  • [K+]o elevations were recorded in the entorhinal cortex during the ictal discharge (peak values = 13.9 +/- 0.9 mM) and the synchronous GABA-mediated potentials (peak values = 4.2 +/- 0.1 mM); the latter increases were presumably attributable to postsynaptic GABAa-receptor activation because they were abolished by DAGO or BMI [30].
  • Exposure to the potent full agonists sufentanil, dihydroetorphine, etorphine, etonitazine, and [D-Ala2, MePhe4, Glyol5]enkephalin (DAMGO) led to strong receptor phosphorylation, while methadone, l-alpha-acetylmethadone (LAAM), morphine, meperidine, DADL, beta-endorphin(1-31), enkephalins, and dynorphin A(1-17) produced intermediate effects [31].
  • Activation of Akt by DAMGO correlates with its phosphorylation at serine 473 [32].
  • Calyculin A increased the magnitude of MOR1TAG phosphorylation without altering the DAMGO-induced loss of the adenylyl cyclase response [4].
 

Gene context of DAMGE

  • Treatment with the mu receptor agonist DAMGO ([d-Ala(2), Me Phe(4), Glyol(5)]enkephalin) led to an increase in PLD2 activity, whereas morphine, which does not induce MOR1 receptor internalization, failed to induce PLD2 activation [33].
  • Our results show that DAMGO administration induces a significant increase in RANTES and IP-10 expression, while MCP-1 protein levels remain unaffected in PBMCs infected with the HIV-1 strain [5].
  • In contrast, we show a dichotomous effect of DAMGO treatment on IP-10 protein levels expressed by T- and M-tropic HIV-infected PBMCs [5].
  • In this report, we show that [D-Ala(2),N:-Me-Phe(4),Gly-ol(5)]enkephalin (DAMGO), a mu-opioid-selective agonist, augments the expression in human PBMCs of MCP-1, RANTES, and IP-10 at both the mRNA and protein levels [5].
  • In the present study, we demonstrate that acute morphine or [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]enkephalin (DAMGO) exposure of COS-7 cells transiently transfected with the micro-opioid receptor and STAT5A, leads to receptor-dependent tyrosine phosphorylation of STAT5A [34].
 

Analytical, diagnostic and therapeutic context of DAMGE

  • This peptide is more effective than the mu-selective analogue DAMGO in vitro and it produces potent and prolonged analgesia in mice [35].
  • Control rats were injected with either saline or a single acute injection of morphine (20 mg/kg). mu opioid-stimulated [35S]GTPgammaS binding was measured by autoradiography of brain sections in the presence and absence of the mu opioid-selective agonist DAMGO [27].
  • Repeated (hourly x 3) intradermal injections of DAMGO or CPA produced tolerance to the antinociceptive effect of a fourth injection 1 hr later [2].
  • Furthermore, the stimulation of mu-opioid receptors by intrathecal perfusion with 10 microM DAGO significantly inhibited the spinal outflow of CGRPLM only in polyarthritic rats [36].
  • In the present study, whole-cell patch-clamp recordings combined with single-cell RT-PCR analysis were used to test the hypothesis that DAMGO ([D-Ala(2),N-methyl-Phe(4),Gly-ol(5)]enkephalin), a specific mu-opioid receptor agonist, selectively hyperpolarizes NRM neurons expressing mRNA of glutamate decarboxylase (GAD(67)) [37].

References

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  2. Opioid and adenosine peripheral antinociception are subject to tolerance and withdrawal. Aley, K.O., Green, P.G., Levine, J.D. J. Neurosci. (1995) [Pubmed]
  3. Mu and delta opiate receptors coupled negatively to adenylate cyclase on embryonic neurons from the mouse striatum in primary cultures. Chneiweiss, H., Glowinski, J., Premont, J. J. Neurosci. (1988) [Pubmed]
  4. The absence of a direct correlation between the loss of [D-Ala2, MePhe4,Gly5-ol]Enkephalin inhibition of adenylyl cyclase activity and agonist-induced mu-opioid receptor phosphorylation. El Kouhen, R., Kouhen, O.M., Law, P.Y., Loh, H.H. J. Biol. Chem. (1999) [Pubmed]
  5. Mu-opioid induction of monocyte chemoattractant protein-1, RANTES, and IFN-gamma-inducible protein-10 expression in human peripheral blood mononuclear cells. Wetzel, M.A., Steele, A.D., Eisenstein, T.K., Adler, M.W., Henderson, E.E., Rogers, T.J. J. Immunol. (2000) [Pubmed]
  6. Prolonged effects of repeated social defeat stress on mRNA expression and function of mu-opioid receptors in the ventral tegmental area of rats. Nikulina, E.M., Miczek, K.A., Hammer, R.P. Neuropsychopharmacology (2005) [Pubmed]
  7. Endogenous morphine modulates acute thermonociception in mice. Guarna, M., Bianchi, E., Bartolini, A., Ghelardini, C., Galeotti, N., Bracci, L., Neri, C., Sonetti, D., Stefano, G. J. Neurochem. (2002) [Pubmed]
  8. Kelatorphan, a potent enkephalinases inhibitor, and opioid receptor agonists DAGO and DTLET, differentially modulate self-stimulation behaviour depending on the site of administration. de Witte, P., Heidbreder, C., Roques, B.P. Neuropharmacology (1989) [Pubmed]
  9. Intake of high-fat food is selectively enhanced by mu opioid receptor stimulation within the nucleus accumbens. Zhang, M., Gosnell, B.A., Kelley, A.E. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  10. mu-Opioid receptor and alpha 2-adrenoceptor agonist binding sites in the postmortem brain of heroin addicts. Gabilondo, A.M., Meana, J.J., Barturen, F., Sastre, M., García-Sevilla, J.A. Psychopharmacology (Berl.) (1994) [Pubmed]
  11. Heterogeneity in presynaptic regulation of GABA release from hippocampal inhibitory neurons. Lambert, N.A., Wilson, W.A. Neuron (1993) [Pubmed]
  12. Sustained potentiation of NMDA receptor-mediated glutamate responses through activation of protein kinase C by a mu opioid. Chen, L., Huang, L.Y. Neuron (1991) [Pubmed]
  13. Opioid receptors from a lower vertebrate (Catostomus commersoni): sequence, pharmacology, coupling to a G-protein-gated inward-rectifying potassium channel (GIRK1), and evolution. Darlison, M.G., Greten, F.R., Harvey, R.J., Kreienkamp, H.J., Stühmer, T., Zwiers, H., Lederis, K., Richter, D. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  14. Purification to homogeneity of an active opioid receptor from rat brain by affinity chromatography. Loukas, S., Mercouris, M., Panetsos, F., Zioudrou, C. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  15. Immunomodulatory activity of mu- and kappa-selective opioid agonists. Taub, D.D., Eisenstein, T.K., Geller, E.B., Adler, M.W., Rogers, T.J. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  16. Kappa- and delta-opioids block sympathetically dependent hyperalgesia. Taiwo, Y.O., Levine, J.D. J. Neurosci. (1991) [Pubmed]
  17. Dissociation of tolerance and dependence for opioid peripheral antinociception in rats. Aley, K.O., Levine, J.D. J. Neurosci. (1997) [Pubmed]
  18. Different mechanisms mediate development and expression of tolerance and dependence for peripheral mu-opioid antinociception in rat. Aley, K.O., Levine, J.D. J. Neurosci. (1997) [Pubmed]
  19. The kappa opioid agonist GR89,696 blocks hyperalgesia and allodynia in rat models of peripheral neuritis and neuropathy. Eliav, E., Herzberg, U., Caudle, R.M. Pain (1999) [Pubmed]
  20. Dopamine and endogenous opioid regulation of picrotoxin-induced locomotion in the ventral pallidum after dopamine depletion in the nucleus accumbens. Churchill, L., Austin, M.C., Kalivas, P.W. Psychopharmacology (Berl.) (1992) [Pubmed]
  21. Locus coeruleus involvement in the learning of classically conditioned bradycardia. Harris, G.C., Fitzgerald, R.D. J. Neurosci. (1991) [Pubmed]
  22. Specific binding of substance P aminoterminal heptapeptide [SP(1-7)] to mouse brain and spinal cord membranes. Igwe, O.J., Kim, D.C., Seybold, V.S., Larson, A.A. J. Neurosci. (1990) [Pubmed]
  23. mu-Opioid receptors modulate NMDA receptor-mediated responses in nucleus accumbens neurons. Martin, G., Nie, Z., Siggins, G.R. J. Neurosci. (1997) [Pubmed]
  24. Inhibitory actions of delta 1-, delta 2-, and mu-opioid receptor agonists on excitatory transmission in lamina II neurons of adult rat spinal cord. Glaum, S.R., Miller, R.J., Hammond, D.L. J. Neurosci. (1994) [Pubmed]
  25. Mu and delta receptors belong to a family of receptors that are coupled to potassium channels. North, R.A., Williams, J.T., Surprenant, A., Christie, M.J. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  26. Dopamine depletion reorganizes projections from the nucleus accumbens and ventral pallidum that mediate opioid-induced motor activity. Churchill, L., Klitenick, M.A., Kalivas, P.W. J. Neurosci. (1998) [Pubmed]
  27. Effects of chronic morphine administration on mu opioid receptor-stimulated [35S]GTPgammaS autoradiography in rat brain. Sim, L.J., Selley, D.E., Dworkin, S.I., Childers, S.R. J. Neurosci. (1996) [Pubmed]
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  29. Highly selective photoaffinity labeling of mu and delta opioid receptors. Garbay-Jaureguiberry, C., Robichon, A., Daugé, V., Rossignol, P., Roques, B.P. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  30. Synchronous GABA-mediated potentials and epileptiform discharges in the rat limbic system in vitro. Avoli, M., Barbarosie, M., Lücke, A., Nagao, T., Lopantsev, V., Köhling, R. J. Neurosci. (1996) [Pubmed]
  31. Mu opioid receptor phosphorylation, desensitization, and ligand efficacy. Yu, Y., Zhang, L., Yin, X., Sun, H., Uhl, G.R., Wang, J.B. J. Biol. Chem. (1997) [Pubmed]
  32. mu-Opioid receptor activates signaling pathways implicated in cell survival and translational control. Polakiewicz, R.D., Schieferl, S.M., Gingras, A.C., Sonenberg, N., Comb, M.J. J. Biol. Chem. (1998) [Pubmed]
  33. ADP-ribosylation factor-dependent phospholipase D2 activation is required for agonist-induced mu-opioid receptor endocytosis. Koch, T., Brandenburg, L.O., Schulz, S., Liang, Y., Klein, J., Hollt, V. J. Biol. Chem. (2003) [Pubmed]
  34. STAT5A interacts with and is phosphorylated upon activation of the mu-opioid receptor. Mazarakou, G., Georgoussi, Z. J. Neurochem. (2005) [Pubmed]
  35. A potent and selective endogenous agonist for the mu-opiate receptor. Zadina, J.E., Hackler, L., Ge, L.J., Kastin, A.J. Nature (1997) [Pubmed]
  36. Increased in vivo release of calcitonin gene-related peptide-like material from the spinal cord in arthritic rats. Collin, E., Mantelet, S., Frechilla, D., Pohl, M., Bourgoin, S., Hamon, M., Cesselin, F. Pain (1993) [Pubmed]
  37. G protein-coupled receptor kinase 2 mediates mu-opioid receptor desensitization in GABAergic neurons of the nucleus raphe magnus. Li, A.H., Wang, H.L. J. Neurochem. (2001) [Pubmed]
 
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