D-ペニシラミン(2,5)-エンケファリン, D-penicillamine(2,5)-enkephalin
English Journal
- Dopamine is differentially involved in the locomotor hyperactivity produced by manipulations of opioid, GABA and glutamate receptors in the median raphe nucleus.
- Shim I1, Stratford TR2, Wirtshafter D3.Author information 1Department of Psychology, University of Illinois at Chicago M/C 285 1007 W. Harrison St., Chicago 60607-7137, IL, U.S.A; AMSRC, Department of Basic Science College of Oriental Medicine, Kyung Hee University, Seoul 130-701, Korea.2Department of Psychology, University of Illinois at Chicago M/C 285 1007 W. Harrison St., Chicago 60607-7137, IL, U.S.A.3Department of Psychology, University of Illinois at Chicago M/C 285 1007 W. Harrison St., Chicago 60607-7137, IL, U.S.A. Electronic address: davew@uic.edu.AbstractThe median raphe nucleus (MR) has been shown to exert a powerful influence on behavioral arousal and marked locomotor hyperactivity can be produced by intra-MR injections of a variety of drugs including GABAA and GABAB agonists, excitatory amino acid antagonists, and μ- and δ-opioid agonists. Other studies have indicated that the MR exerts an inhibitory influence on ascending dopamine systems, suggesting that MR induced alterations in activity may be mediated through changes in dopaminergic transmission. In the present study, we explored this possibility by examining whether systemic administration of the preferential D2 dopamine antagonist haloperidol is able to antagonize the hyperactivity produced by intra-MR injections of various drugs. We found that haloperidol completely blocked the locomotor response to intra-MR injections of the μ-opioid receptor agonist DAMGO and the δ-opioid receptor agonist DPDPE. In marked contrast, at doses which abolished the locomotor response to systemic amphetamine, haloperidol had no effect on the hyperactivity induced by intra-MR injections of GABAA agonist muscimol, the GABAB agonist baclofen, or the kainate/quisqualate antagonist pBB-PZDA, even though it suppressed baseline activity in these same animals. These results indicate that there must be at least two mechanisms capable of influencing behavioral arousal within the MR region, one of which is dependent on D2 dopamine receptors and the other is not.
- Behavioural brain research.Behav Brain Res.2014 Mar 15;261:65-70. doi: 10.1016/j.bbr.2013.12.004. Epub 2013 Dec 12.
- The median raphe nucleus (MR) has been shown to exert a powerful influence on behavioral arousal and marked locomotor hyperactivity can be produced by intra-MR injections of a variety of drugs including GABAA and GABAB agonists, excitatory amino acid antagonists, and μ- and δ-opioid agonists. Othe
- PMID 24333380
- δ-Opioid receptor activation stimulates normal diet intake but conversely suppresses high-fat diet intake in mice.
- Kaneko K1, Mizushige T, Miyazaki Y, Lazarus M, Urade Y, Yoshikawa M, Kanamoto R, Ohinata K.Author information 1Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Gokasho Uji, Kyoto, Japan;AbstractThe central opioid system is involved in a broadly distributed neural network that regulates food intake. Here, we show that activation of central δ-opioid receptor not only stimulated normal diet intake but conversely suppressed high-fat diet intake as well. [d-Pen(2,5)]-enkephalin (DPDPE), an agonist selective for the δ-receptor, increased normal diet intake after central administration to nonfasted male mice. The orexigenic activity of DPDPE was inhibited by blockade of cyclooxygenase (COX)-2, lipocalin-type prostaglandin D synthase (L-PGDS), D-type prostanoid receptor 1 (DP1), and neuropeptide Y (NPY) receptor type 1 (Y1) for PGD2 and NPY, respectively, suggesting that this was mediated by the PGD2-NPY system. In contrast, DPDPE decreased high-fat diet intake in mice fed a high-fat diet. DPDPE-induced suppression of high-fat diet intake was blocked by antagonists of melanocortin 4 (MC4) and corticotropin-releasing factor (CRF) receptors but not by knockout of the L-PGDS gene. These results suggest that central δ-opioid receptor activation suppresses high-fat diet intake via the MC-CRF system, independent of the orexigenic PGD2 system. Furthermore, orally administered rubiscolin-6, an opioid peptide derived from spinach Rubisco, suppressed high-fat diet intake. This suppression was also blocked by centrally administered naltrindole, an antagonist for the δ-receptor, suggesting that rubiscolin-6 suppressed high-fat diet intake via activation of central δ-opioid receptor.
- American journal of physiology. Regulatory, integrative and comparative physiology.Am J Physiol Regul Integr Comp Physiol.2014 Feb;306(4):R265-72. doi: 10.1152/ajpregu.00405.2013. Epub 2014 Jan 8.
- The central opioid system is involved in a broadly distributed neural network that regulates food intake. Here, we show that activation of central δ-opioid receptor not only stimulated normal diet intake but conversely suppressed high-fat diet intake as well. [d-Pen(2,5)]-enkephalin (DPDPE), an ago
- PMID 24401991
- LY2456302 is a novel, potent, orally-bioavailable small molecule kappa-selective antagonist with activity in animal models predictive of efficacy in mood and addictive disorders.
- Rorick-Kehn LM1, Witkin JM2, Statnick MA2, Eberle EL2, McKinzie JH2, Kahl SD2, Forster BM2, Wong CJ2, Li X2, Crile RS2, Shaw DB2, Sahr AE2, Adams BL2, Quimby SJ2, Diaz N2, Jimenez A2, Pedregal C2, Mitch CH2, Knopp KL2, Anderson WH2, Cramer JW2, McKinzie DL2.Author information 1Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN 46285, USA. Electronic address: rorickkehnlm@lilly.com.2Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN 46285, USA.AbstractKappa opioid receptors and their endogenous neuropeptide ligand, dynorphin A, are densely localized in limbic and cortical areas comprising the brain reward system, and appear to play a key role in modulating stress and mood. Growing literature indicates that kappa receptor antagonists may be beneficial in the treatment of mood and addictive disorders. However, existing literature on kappa receptor antagonists has used extensively JDTic and nor-BNI which exhibit long-lasting pharmacokinetic properties that complicate experimental design and interpretation of results. Herein, we report for the first time the in vitro and in vivo pharmacological profile of a novel, potent kappa opioid receptor antagonist with excellent selectivity over other receptors and markedly improved drug-like properties over existing research tools. LY2456302 exhibits canonical pharmacokinetic properties that are favorable for clinical development, with rapid absorption (t(max): 1-2 h) and good oral bioavailability (F = 25%). Oral LY2456302 administration selectively and potently occupied central kappa opioid receptors in vivo (ED₅₀ = 0.33 mg/kg), without evidence of mu or delta receptor occupancy at doses up to 30 mg/kg. LY2456302 potently blocked kappa-agonist-mediated analgesia and disruption of prepulse inhibition, without affecting mu-agonist-mediated effects at doses >30-fold higher. Importantly, LY2456302 did not block kappa-agonist-induced analgesia one week after administration, indicating lack of long-lasting pharmacodynamic effects. In contrast to the nonselective opioid antagonist naltrexone, LY2456302 produced antidepressant-like effects in the mouse forced swim test and enhanced the effects of imipramine and citalopram. LY2456302 reduced ethanol self-administration in alcohol-preferring (P) rats and, unlike naltrexone, did not exhibit significant tolerance upon 4 days of repeated dosing. LY2456302 is a centrally-penetrant, potent, kappa-selective antagonist with pharmacokinetic properties favorable for clinical development and activity in animal models predictive of efficacy in mood and addictive disorders.
- Neuropharmacology.Neuropharmacology.2014 Feb;77:131-44. doi: 10.1016/j.neuropharm.2013.09.021. Epub 2013 Sep 23.
- Kappa opioid receptors and their endogenous neuropeptide ligand, dynorphin A, are densely localized in limbic and cortical areas comprising the brain reward system, and appear to play a key role in modulating stress and mood. Growing literature indicates that kappa receptor antagonists may be benefi
- PMID 24071566
Japanese Journal
- Increase of Calmodulin III Gene Expression by μ-Opioid Receptor Stimulation in PC12 Cells
- NIU Sanyoung,KUO Che-Hui,GAN Yehua,NISHIKAWA Etsuko,SADAKATA Tetsushi,ICHIKAWA Hisashi,MIKI Naomasa
- The Japanese journal of pharmacology 84(4), 412-417, 2000-12-01
- … The expression was also increased with DAMGO (μ-opioid agonist), but not by DPDPE (δ) and U50488 (κ). …
- NAID 10008186655
- A DPDPE-induced enhancement of inward rectifier potassium current via poioid receptor in neuroblastoma x glioma NG108-15 cells
- SHI YuLiang,HUANG FenSheng,CHEN WenYan,WU Ying,TANG Yun,HU Qian
- Neuroscience research : the official journal of the Japan Neuroscience Society 36(3), 209-214, 2000-03
- NAID 10006156761
- Inhibition by Naloxone of Promoter Activity of the Neurofilament Gene in SK-N-SH Cells
- NIU San-Yong,KUO Che-Hui,TAIRA Eiichi,MURAOKA Osamu,IRIE Yasuyuki,GAN Ye-Hua,DO Eunju,MIKI Naomasa
- The Japanese journal of pharmacology 82(1), 34-39, 2000-01-01
- … M suppressed the promoter activity about 20%, but levallorphan, DAMGO, DPDPE and U50488 did not.The inhibition by naloxone was dose−dependent and not reversed by morphine.The inhibitory effect of naloxone was not observed in N18TG−2 cells and PC12 cells.Experiments with various deletion mutants revealed that a region responsible for naloxone suppression spans from −328 to − 101 in the gene.These results suggest that naloxone has the ability to suppress transcriptional activity in some neurons. …
- NAID 10008182601
Related Links
- View and buy high purity DPDPE from Tocris Bioscience, the leading worldwide supplier of high performance life science reagents ... References Clark et al (1986) [D-Pen 2,D-Pen 5]enkephalin (DPDPE): a δ-selective enkephalin with ...
- What is the meaning of DPDPE acronym/abbreviation and what does DPDPE stand for? Get the Definition of DPDPE and DPDPE definition by All Acronyms Dictionary - 1 DPDPE acronym and abbreviation record for your search.
Related Pictures
★リンクテーブル★
| リンク元 | 「オピオイド」「D-ペニシラミン(2,5)-エンケファリン」「D-penicillamine(2,5)-enkephalin」 |
| 関連記事 | 「DPD」 |
「オピオイド」
- 内因性のオピオイドペプチドが発見され、これらは内因性オピオイドペプチドと呼ばれるようになった。
作用
縮瞳
- モルフィンと多くのμ,κアゴニストは瞳孔の縮小を引き起こす。これは瞳孔を支配する副交感神経の興奮による。μアゴニストを中毒量投与すると縮瞳し、pinpoints pupupilsはpathognomonicである。(GOO.559)
オピオイドとオピオイド類似物質の作用
- GOO.552
| Drugs | RECEPTOR TYPES | ||
| μ受容体 | δ受容体 | κ受容体 | |
| morphine | ＋＋＋ | ＋ | |
| methadone | ＋＋＋ | ||
| etorphine | ＋＋＋ | ＋＋＋ | ＋＋＋ |
| levorphanol | ＋＋＋ | ||
| fentanyl | ＋＋＋ | ||
| sufentanil | ＋＋＋ | ＋ | ＋ |
| DAMGO | ＋＋＋ | ||
| butorphanol | P | ＋＋＋ | |
| buprenorphine | P | ーー | |
| naloxone | ーーー | ー | ーー |
| naltrexone | ーーー | ー | ーーー |
| CTOP | ーーー | ||
| diprenorphine | ーーー | ーー | ーーー |
| β-funaltrexamine | ーーー | ー | ＋＋ |
| naloxonazine | ーーー | ー | ー |
| nalorphine | ーーー | ＋ | |
| pentazocine | P | ＋＋ | |
| nalbuphine | ーー | ＋＋ | |
| naloxone benzoylhydrazone | ーーー | ー | ー |
| bremazocine | ＋＋＋ | ＋＋ | ＋＋＋ |
| ethylketocyclazocine | P | ＋ | ＋＋＋ |
| U50,488 | ＋＋＋ | ||
| U69,593 | ＋＋＋ | ||
| spiradoline | ＋ | ＋＋＋ | |
| nor-Binaltorphimine | ー | ー | ーーー |
| naltrindole | ー | ーーー | ー |
| DPDPE | ＋＋ | ||
| [[［[D-Ala2,Glu4］deltorphin]] | ＋＋ | ||
| DSLET | ＋ | ＋＋ | |
| endogenous Peptides | |||
| met-enkephalin | ＋＋ | ＋＋＋ | |
| leu-enkephalin | ＋＋ | ＋＋＋ | |
| β-endorphin | ＋＋＋ | ＋＋＋ | |
| dynorphin A | ＋＋ | ＋＋＋ | |
| dynorphin B | ＋ | ＋ | ＋＋＋ |
| α-neoendorphin | ＋ | ＋ | ＋＋＋ |
＋アゴニスト ーアンタゴニスト P partial agonist
各鎮痛薬のオピオイド受容体への作用
- μ受容体 κ受容体
- レミフェンタニル ＋＋＋ ー
- フェンタニル ＋＋＋ －
- モルヒネ ＋＋＋ ＋
- ペチジン ＋＋ ＋
- トラマドール ＋ －
- ペンタゾシン ー ＋＋
- ブプレノルフィン Ｐ ー
- ナロキソン ー －
「D-ペニシラミン(2,5)-エンケファリン」
- 英
- D-penicillamine (2,5)-enkephalin、DPDPE
「D-penicillamine(2,5)-enkephalin」
D-ペニシラミン(2
- 関
- DPDPE