n.

オピエート、アヘン剤。(広義)麻酔薬、鎮痛薬。[fig](感覚を)鈍くするもの

adj.

アヘンの、阿片を含む。アヘン剤の、麻酔薬の。催眠/鎮静の。麻酔する

vt.

WordNet

a narcotic drug that contains opium or an opium derivative

PrepTutorEJDIC

アヘン剤,鎮静剤 / (…にとって)鎮静させるもの《+『to』+『名』》 / アヘンを用いた;鎮静の

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/06/16 00:14:44」(JST)

wiki en

[Wiki en表示]

Harvesting the poppy pod.

Opiates are alkaloid compounds found naturally in the opium poppy plant Papaver somniferum.^[1] The psychoactive compounds found in the opium plant include morphine, codeine, and thebaine. The term opiate should be differentiated from the broader term opioid, which includes all drugs with morphine-like effects, including opiates, semi-synthetic opioids derived from opiates (such as heroin, hydrocodone, hydromorphone, oxycodone, and oxymorphone),^[2] and synthetic opioids which are not derived from opiates (such as fentanyl, buprenorphine, and methadone). All opioids, including the opiates, are considered drugs of high abuse potential and are listed on various "Substance-Control Schedules" under the Uniform Controlled Substances Act of the United States.

In 2013 between 13 and 20 million people used opiates recreationally (0.3% to 0.4% of the global population between the ages of 15 and 65).^[3]

Overview

Codeine

Chemical structure of morphine

Opiates belong to the large biosynthetic group of benzylisoquinoline alkaloids, and are so named because they are naturally occurring alkaloids found in the opium poppy. The major psychoactive opiates are morphine, codeine, and thebaine. Papaverine, noscapine, and approximately 24 other alkaloids are also present in opium but have little to no effect on the human central nervous system, and as such are not considered to be opiates. Very small quantities of hydrocodone and hydromorphone are detected in assays of opium on rare occasions; it appears to be produced by the plant under circumstances and by processes which are not understood at this time and may include the action of bacteria.^{[citation needed]} Dihydrocodeine, oxymorphol, oxycodone, oxymorphone, metopon and possibly other derivatives of morphine and/or hydromorphone also are found in trace amounts in opium.^{[citation needed]}

Despite morphine being the most medically significant opiate, larger quantities of codeine are consumed medically, most of it synthesized from morphine. Codeine has greater and more predictable oral bioavailability, making it easier to titrate the dose. Codeine also has less abuse potential than morphine, and because it is milder, larger doses of codeine are required.^[4]

Withdrawal effects

Morphine addiction cure advertisement in the year 1900

Opiate withdrawal syndrome effects are associated with the abrupt cessation or reduction of prolonged opiate usage.

In medical facilities such as hospitals and clinics, the threat of relapse is possible when Post-acute-withdrawal syndrome is under-emphasized to patients in transitional phases, especially with short-term buprenorphine, methadone or health facilities.

Synthesis

While the full synthesis of opioids from naphthoquinone (Gates synthesis) or other simple organic starting materials is possible, they are tedious and uneconomical processes. Therefore, most of the opiate-type analgesics in use today are either extracted from Papaver somniferum or synthesized from those opiates, especially thebaine.^[5]

In 2015 researches reported successful biosynthesis of thebaine and hydrocodone using genetically modified yeast. Once scaled for commercial use the process would cut production time from a year to several days and could reduce costs by 90%.^[6]^[7]

Esters of morphine

Heroin is one of several semi-synthetic opioids derived from the morphine. Heroin (diacetylmorphine) is a morphine prodrug; it is metabolized by into morphine after administration. One of the major metabolites of heroin, 6-monoacetylmorphine (6-MAM), is also a morphine prodrug. Nicomorphine (morphine dinicotinate), dipropanoylmorphine (morphine dipropionate), desomorphine (di-hydro-desoxy-morphine), methyldesorphine, acetylpropionylmorphine, dibenzoylmorphine, diacetyldihydromorphine, and several others are also derived from morphine.^[8]

References

^ "Opiate - Definitions from Dictionary.com". dictionary.reference.com. Retrieved 2008-07-04.
^ Levine, Barry (2003-01-01). Principles of Forensic Toxicology. Amer. Assoc. for Clinical Chemistry. pp. 198–201. ISBN 9781890883874. Dihydrocodeine … [is a derivative] of codeine.... Heroin … is obtained synthetically … from morphine…. Hydrocodone is … derived from codeine…. Oxycodone is … derived from thebaine…. Oxymorphone is … derived from thebaine.
^ "Status and Trend Analysis of Illict [sic] Drug Markets". World Drug Report 2015 (pdf). Retrieved 26 June 2015.
^ "Canadian Guideline for Opioid Use for Pain — Appendix B-8: Opioid Conversion and Brand Availability in Canada". nationalpaincentre.mcmaster.ca. Retrieved 2016-04-18.
^ Synthesis of morphine alkaloids Presentation School of Chemical Sciences, University of Illinois at Urbana-Champaign retrieved 12-02-2010
^ Galanie, Stephanie; Thodey, Kate; Trenchard, Isis J.; Interrante, Maria Filsinger; Smolke, Christina D. (2015-09-04). "Complete biosynthesis of opioids in yeast". Science 349 (6252): 1095–1100. doi:10.1126/science.aac9373. ISSN 0036-8075. PMID 26272907.
^ Mobley, Emily (2015-08-13). "Yeast cells genetically modified to create morphine-like painkiller". The Guardian. ISSN 0261-3077. Retrieved 2016-04-17.
^ "Esters of Morphine". www.unodc.org. United Nations Office on Drugs and Crime. Retrieved 10 March 2012.

External links

World Health Organization guidelines for the availability and accessibility of controlled substances

UpToDate Contents

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1. 慢性疼痛の治療の概要 overview of the treatment of chronic pain
2. オピオイド使用障害：疫学、薬理学、臨床症状、経過、スクリーニング、評価、および診断 opioid use disorder epidemiology pharmacology clinical manifestations course screening assessment and diagnosis
3. 成人における急性オピオイド中毒 acute opioid intoxication in adults
4. Pharmacotherapy for opioid use disorder
5. オピオイド系薬剤を用いた癌疼痛のマネージメント：至適鎮痛作用 cancer pain management with opioids optimizing analgesia

English Journal

Extinction of opiate reward reduces dendritic arborization and c-Fos expression in the nucleus accumbens core.

Leite-Morris KA1, Kobrin KL2, Guy MD3, Young AJ4, Heinrichs SC5, Kaplan GB6.Author information 1Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Psychiatry, Boston University School of Medicine, 720 Harrison Avenue, Boston, Massachusetts, 02118, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: kleitemo@bu.edu.2Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: kendrak@bu.edu.3Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: marsha.guy@gmail.com.4Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: angela.pieroniyoung@facebook.com.5Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: Stephen.Heinrichs@va.gov.6Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Mental Health Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Psychiatry, Boston University School of Medicine, 720 Harrison Avenue, Boston, Massachusetts, 02118, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: Gary.Kaplan@va.gov.AbstractRecurrent opiate use combined with environmental cues, in which the drug was administered, provokes cue-induced drug craving and conditioned drug reward. Drug abuse craving is frequently linked with stimuli from a prior drug-taking environment via classical conditioning and associative learning. We modeled the conditioned morphine reward process by using acquisition and extinction of conditioned place preference (CPP) in C57BL/6 mice. Mice were trained to associate a morphine injection with a drug context using a classical conditioning paradigm. In morphine conditioning (0, 0.25, 0.5, 1, 5, or 10mg/kg) experimental mice acquired a morphine CPP dose response with 10mg/kg as most effective. During morphine CPP extinction experiments, mice were divided into three test groups: morphine CPP followed by extinction training, morphine CPP followed by sham extinction, and saline controls. Extinction of morphine CPP developed within one extinction experiment (4 days) that lasted over two more trials (another 8 days). However, the morphine CPP/sham extinction group retained a place preference that endured through all three extinction trials. Brains were harvested following CPP extinction and processed using Golgi-Cox impregnation. Changes in dendritic morphology and spine quantity were examined in the nucleus accumbens (NAc) Core and Shell neurons. In the NAcCore only, morphine CPP/extinguished mice produced less dendritic arborization, and a decrease in neuronal activity marker c-Fos compared to the morphine CPP/sham extinction group. Extinction of morphine CPP is associated with decreased structural complexity of dendrites in the NAcCore and may represent a substrate for learning induced structural plasticity relevant to addiction.
Behavioural brain research.Behav Brain Res.2014 Apr 15;263:51-9. doi: 10.1016/j.bbr.2013.12.041. Epub 2014 Jan 7.
Recurrent opiate use combined with environmental cues, in which the drug was administered, provokes cue-induced drug craving and conditioned drug reward. Drug abuse craving is frequently linked with stimuli from a prior drug-taking environment via classical conditioning and associative learning. We
PMID 24406724

Morphine-induced trafficking of a mu-opioid receptor interacting protein in rat locus coeruleus neurons.

Jaremko KM1, Thompson NL Jr1, Reyes BA2, Jin J3, Ebersole B3, Jenney CB4, Grigson PS4, Levenson R3, Berrettini WH5, Van Bockstaele EJ1.Author information 1Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States.2Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States. Electronic address: Beverly.Reyes@drexelmed.edu.3Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033, United States.4Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, PA 17033, United States.5Department of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, United States.AbstractOpiate addiction is a devastating health problem, with approximately 2million people currently addicted to heroin or non-medical prescription opiates in the United States alone. In neurons, adaptations in cell signaling cascades develop following opioid actions at the mu opioid receptor (MOR). A novel putative target for intervention involves interacting proteins that may regulate trafficking of MOR. Morphine has been shown to induce a re-distribution of a MOR-interacting protein Wntless (WLS, a transport molecule necessary for secretion of neurotrophic Wnt proteins), from cytoplasmic to membrane compartments in rat striatal neurons. Given its opiate-sensitivity and its well-characterized molecular and cellular adaptations to morphine exposure, we investigated the anatomical distribution of WLS and MOR in the rat locus coeruleus (LC)-norepinephrine (NE) system. Dual immunofluorescence microscopy was used to test the hypothesis that WLS is localized to noradrenergic neurons of the LC and that WLS and MOR co-exist in common LC somatodendritic processes, providing an anatomical substrate for their putative interactions. We also hypothesized that morphine would influence WLS distribution in the LC. Rats received saline, morphine or the opiate agonist [d-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO), and tissue sections through the LC were processed for immunogold-silver detection of WLS and MOR. Statistical analysis showed a significant re-distribution of WLS to the plasma membrane following morphine treatment in addition to an increase in the proximity of gold-silver labels for MOR and WLS. Following DAMGO treatment, MOR and WLS were predominantly localized within the cytoplasmic compartment when compared to morphine and control. In a separate cohort of rats, brains were obtained from saline-treated or heroin self-administering male rats for pulldown co-immunoprecipitation studies. Results showed an increased association of WLS and MOR following heroin exposure. As the LC-NE system is important for cognition as well as decisions underlying substance abuse, adaptations in WLS trafficking and expression may play a role in modulating MOR function in the LC and contribute to the negative sequelae of opiate exposure on executive function.
Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2014 Apr 3;50:53-65. doi: 10.1016/j.pnpbp.2013.12.003. Epub 2013 Dec 12.
Opiate addiction is a devastating health problem, with approximately 2million people currently addicted to heroin or non-medical prescription opiates in the United States alone. In neurons, adaptations in cell signaling cascades develop following opioid actions at the mu opioid receptor (MOR). A nov
PMID 24333843

Morphine modulates cell proliferation through mir133b &mir128 in the neuroblastoma SH-SY5Y cell line.

Gonzalez-Nunez V1, Noriega-Prieto JA2, Rodríguez RE3.Author information 1Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Salamanca, Spain; Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain.2Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain.3Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Salamanca, Spain; Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain. Electronic address: requelmi@usal.es.AbstractNeuroblastoma is a childhood cancer with high incidence and high mortality rate. Great efforts are made to find new treatments and molecular markers for diagnosis and prognosis. miRNAs stand for novel strategies to modulate tumor growth, as they can act either as tumor suppressors or as oncogenes. Morphine is an opioid agonist widely used to treat severe and chronic pain, as for example cancer pain. Previous studies have revealed that morphine is able to modify cancer progression, by acting on proliferation or on apoptosis; however, up to date, the available results are contradictory, maybe due to the different doses used, routes of administration and model systems. While some studies show that morphine promotes cell proliferation and metastasis, other authors sustain that morphine effect is mainly antiproliferative and pro-apoptotic. In this study we aim to establish the effect of chronic opiate administration on cell proliferation in the neuroblastoma SH-SY5Y cell line. Low doses of morphine (10nM) promoted cell proliferation in undifferentiated cells and reduced the expression levels of miR133b, while higher doses (1μM) inhibited cell proliferation and correlated with decreased levels of miR133b and miR128 without triggering apoptosis. Naloxone, the classical opioid antagonist, could not fully block the effect of morphine on miR128 expression, so that the observed effect may be mediated by non-opioid mechanisms. Our results represent a further contribution to the hypothesis that a joint regulation of miRNA networks and the specific characteristics of the target tissue may determine the effect of morphine on tumor cell growth.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Apr;1842(4):566-72. doi: 10.1016/j.bbadis.2014.01.003. Epub 2014 Jan 14.
Neuroblastoma is a childhood cancer with high incidence and high mortality rate. Great efforts are made to find new treatments and molecular markers for diagnosis and prognosis. miRNAs stand for novel strategies to modulate tumor growth, as they can act either as tumor suppressors or as oncogenes. M
PMID 24440526

Duration of opiate exposure as a determinant of arterial stiffness and vascular age in male opiate dependence: a longitudinal study.

Reece AS1, Hulse GK.Author information 1School of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, WA, Australia.AbstractWHAT IS KNOWN AND OBJECTIVE: Despite intriguing initial and associational studies, there remains little research on opiate-related arterial dysfunction and no longitudinal studies. As opiates act potently via P16INK4A/CDKN2A identified on GWAS screens, and as arterial ageing is a surrogate for organismal ageing, this area is of general concern.
Journal of clinical pharmacy and therapeutics.J Clin Pharm Ther.2014 Apr;39(2):158-67. doi: 10.1111/jcpt.12121. Epub 2013 Dec 16.
WHAT IS KNOWN AND OBJECTIVE: Despite intriguing initial and associational studies, there remains little research on opiate-related arterial dysfunction and no longitudinal studies. As opiates act potently via P16INK4A/CDKN2A identified on GWAS screens, and as arterial ageing is a surrogate for organ
PMID 24329809

Japanese Journal

A personal view from a long-lasting collaborator on the research strategies of Marshall Nirenberg

Higashida Haruhiro
Neurochemistry International 61(6), 821-827, 2012-11
… Especially he liked his hypothesis for opiate tolerance and dependency as a model of cellular memory. …
NAID 120004966606

Inhibition of Morphine Glucuronidation in the Liver Microsomes of Rats and Humans by Monoterpenoid Alcohols

Ishii Yuji,Iida Naoko,Miyauchi Yuu [他],Mackenzie Peter I.,Yamada Hideyuki
Biological and Pharmaceutical Bulletin 35(10), 1811-1817, 2012
… This opiate is mainly metabolized by glucuronidation to a non-analgesic metabolite, morphine-3-glucuronide (M-3-G) and an active metabolite morphine-6-glucuronide (M-6-G). …
NAID 130001872386

Perforation of Peptic Ulcer Following Abrupt Cessation of Long-term Opiate Use

KAHROM MAHDI,KAHROM HADI
Surgery today : the Japanese journal of surgery 40(9), 836-839, 2010-09-01
NAID 10027397617

FACT誌収載鍼灸関係論文(114)耳介鍼療法(auricular acupuncture)はオピエイトの禁断症状のひどさを軽減しない

直本美知 [訳],濱田淳 [訳]
医道の日本 69(8), 68-70, 2010-08
NAID 40017246802

Related Pictures

★リンクテーブル★

リンク元	「意識障害」「アヘン」「オピエート」
拡張検索	「opiate dependence」「opiate addiction」「opiate receptor」
関連記事	「opia」

「意識障害」

　　[★]

英: consciousness disturbance, disturbance of consciousness
関: 意識

分類

時間による分類

急性/慢性, 持続性/一過性

急性＋一過性：失神、てんかん
慢性＋持続性：植物状態、認知症

PSY.38

単純な意識障害

明識困難状態 < 昏蒙 < 傾眠 < 昏眠 < 昏睡

複雑な意識障害

せん妄　　　　　意識混濁　＋　(高度)精神運動興奮

振戦せん妄

作業せん妄

夜間せん妄

もうろう状態　　意識狭窄　＋　(軽度)精神運動興奮
アメンチア

意識障害に関連した特殊な病態

意識レベルの分類覚醒度

Mayo Clinicの分類

救急意識障害をみたら

AIUEOTIPS (also see DIF.96)

	症候学プリント		DIF.95
A	alcohol	アルコール関連	accidents, arterial occlusions, arteriosclerosis, aneurysms, autoimmune disorders
I	insulin	インスリン関連(低血糖、糖尿病性ケトアシドーシス、非ケトン性高浸透圧性昏睡)	inflammatory, intoxication (encephalitis, cerebral abcess, meningitis, alcoholism, opiates, barbiturates)
U	uremia	尿毒症、電解質異常、内分泌異常、肝性脳症	undefined disorders (narcolepsy, conversion hysteria)
E	encephalopathy, endocrinopathy, electrolyte	脳症(脳炎、脳血管障害)、てんかん後	endocrine disorders(myxedema coma, hyperparathyroidism, diabetic coma, insulin shock), epileptic coma
O	opiate, other overdose of O2 & CO2	薬物中毒	organ failure(hepatic coma, respiratory failure, uremia)
T	trauma, tumor, temparature	頭部外傷、脳挫傷、硬膜外血腫、硬膜下血腫
I	infection	感染症、髄膜炎
P	psychogenic	精神疾患
S	syncope, seizure, stroke, shock, senile	失神、クモ膜下出血