WordNet
- used to express refusal or denial or disagreement etc or especially to emphasize a negative statement; "no, you are wrong"
- a negative; "his no was loud and clear"
- referring to the degree to which a certain quality is present; "he was no heavier than a child" (同)no more
- not in any degree or manner; not at all; "he is no better today"
- quantifier; used with either mass nouns or plural count nouns for indicating a complete or almost complete lack or zero quantity of; "we have no bananas"; "no eggs left and no money to buy any"; "have you no decency?"; "did it with no help"; "Ill get you there in no time"
PrepTutorEJDIC
- 《名詞の前に置いて》『一つも』(『一人も,少しも』)・・・『ない』 / 《補語につけて》『決して・・・でない』 / 《省略文で》・・・なし;・・・お断り / 《話》少ししか(あまり)・・・ない / (肯定の問いに対して)『いいえ』;(否定の問いに対して)はい,ええ / 《not, norの前に挿入して》『いや』,否 / 《形容詞の前に置その形容詞を否定して》…どころではない / 《比較級の前に置いて》ちっとも…でない,…と全く同じ / 《… or no の形で》…であってもなくても / 《驚き・困惑・不信などを表して》とんでもない / 《単数形で》『拒否』,「『いいえ』」という返事 / 《複数形で》反対[投]票
- 《neither…nor,で》…『も』,『も』…『ない』,また…ない(or not) / 《not,no,neverなどを含む否定節の後で,さらに次に続く内容を否定して》…『もまた』…『ない』 / 《肯定文の後,または文頭に置いて,次に続く内容を否定して》『そしてまた』…『ない』(and not)
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/10/28 23:46:08」(JST)
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- 1. ジゴキシン中毒患者におけるジゴキシン特異的抗体（Fab）フラグメントに対する投与レジメン dosing regimen for digoxin specific antibody fab fragments in patients with digoxin toxicity
- 2. ヨード造影剤による甲状腺機能亢進症の治療 iodinated radiocontrast agents in the treatment of hyperthyroidism
- 3. 肺の大細胞神経内分泌癌 large cell neuroendocrine carcinoma of the lung
- 4. 潜在結核感染診断のためのインターフェロン遊離試験（IGRA） interferon gamma release assays for diagnosis of latent tuberculosis infection
- 5. Autism and chronic disease: No evidence for vaccines as a contributing factor
English Journal
- Kappa opioid receptor activation decreases inhibitory transmission and antagonizes alcohol effects in rat central amygdala.
- Gilpin NW1, Roberto M2, Koob GF2, Schweitzer P3.Author information 1Department of Physiology, Louisiana State University, Health Sciences Center, 1901 Perdido Street, New Orleans, LA 70130, USA.2Committee on the Neurobiology of Addictive Disorders & Pearson Center for Alcoholism and Addiction Research, SP30 2400, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.3Committee on the Neurobiology of Addictive Disorders & Pearson Center for Alcoholism and Addiction Research, SP30 2400, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: pschweitzer@scripps.edu.AbstractActivation of the kappa opioid receptor (KOR) system mediates negative emotional states and considerable evidence suggests that KOR and their natural ligand, dynorphin, are involved in ethanol dependence and reward. The central amygdala (CeA) plays a major role in alcohol dependence and reinforcement. Dynorphin peptide and gene expression are activated in the amygdala during acute and chronic administration of alcohol, but the effects of activation or blockade of KOR on inhibitory transmission and ethanol effects have not been studied. We used the slice preparation to investigate the physiological role of KOR and interaction with ethanol on GABA(A) receptor-mediated synaptic transmission. Superfusion of dynorphin or U69593 onto CeA neurons decreased evoked inhibitory postsynaptic potentials (IPSPs) in a concentration-dependent manner, an effect prevented by the KOR antagonist norbinaltorphimine (norBNI). Applied alone, norBNI increased GABAergic transmission, revealing a tonic endogenous activity at KOR. Paired-pulse analysis suggested a presynaptic KOR mechanism. Superfusion of ethanol increased IPSPs and pretreatment with KOR agonists diminished the ethanol effect. Surprisingly, the ethanol-induced augmentation of IPSPs was completely obliterated by KOR blockade. Our results reveal an important role of the dynorphin/KOR system in the regulation of inhibitory transmission and mediation of ethanol effects in the CeA.
- Neuropharmacology.Neuropharmacology.2014 Feb;77:294-302. doi: 10.1016/j.neuropharm.2013.10.005. Epub 2013 Oct 21.
- Activation of the kappa opioid receptor (KOR) system mediates negative emotional states and considerable evidence suggests that KOR and their natural ligand, dynorphin, are involved in ethanol dependence and reward. The central amygdala (CeA) plays a major role in alcohol dependence and reinforcemen
- PMID 24157490
- Pain-Related Depression of the Mesolimbic Dopamine System in Rats: Expression, Blockade by Analgesics, and Role of Endogenous κ-opioids.
- Leitl MD1, Onvani S2, Bowers MS3, Cheng K4, Rice KC4, Carlezon WA Jr2, Banks ML1, Negus SS1.Author information 1Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, USA.2Behavioral Genetics Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA, USA.3Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA.4Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.AbstractPain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats.
- Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology.Neuropsychopharmacology.2014 Feb;39(3):614-24. doi: 10.1038/npp.2013.236. Epub 2013 Sep 6.
- Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimb
- PMID 24008352
- Cocaine- or stress-induced metaplasticity of LTP in the dorsal and ventral hippocampus.
- Keralapurath MM, Clark J, Hammond S, Wagner JJ.Author information Department of Physiology & Pharmacology, University of Georgia, Athens, USA; Interdisciplinary Toxicology Program, University of Georgia, Athens, USA.AbstractDespite the well documented role of the hippocampus in various modes of drug reinstatement behavior, the persisting effects of in vivo cocaine exposure on hippocampal synaptic plasticity are not sufficiently understood. In this report we investigated the effects of cocaine conditioning on long-term potentiation (LTP) in the CA1 region of hippocampus along its septotemporal axis. Male Sprague Dawley rats experienced a behavioral protocol in which locomotor activity was monitored in response to various conditioning treatments. LTP was measured in ex vivo slice preparations taken 1-2 weeks after the last behavioral session from the ventral (vH) and dorsal (dH) sectors of hippocampus. Unexpectedly, experiencing the minor intermittent stimuli of the behavioral protocol caused stress-induced metaplastic changes in both vH (increased LTP) and dH (decreased LTP) in the saline conditioned rats relative to behaviorally naïve controls. These stress effects in the vH and dH were blocked by conditioning with either mineralocorticoid (spironolactone) or glucocorticoid (mifepristone) antagonists, respectively. Stress-induced metaplasticity in the vH was also prevented by prior administration of the kappa opioid antagonist nor-binaltorphimine. Cocaine conditioning induced locomotor sensitization and significantly increased LTP in the vH without causing significant change in LTP in the dH. Cocaine-induced metaplasticity in the vH was prevented by co-administration of the dopamine D2-like antagonist eticlopride during cocaine conditioning, but not by co-administration of the D1/5 antagonist SCH 23390. Our results suggest that the functional connectivity of hippocampus is altered by metaplastic triggers such as exposure to drugs of abuse and/or stressors, thereby shifting the efferent output of hippocampus from dH (cortical) towards vH (limbic) influenced circuits. © 2014 Wiley Periodicals, Inc.
- Hippocampus.Hippocampus.2014 Jan 27. doi: 10.1002/hipo.22250. [Epub ahead of print]
- Despite the well documented role of the hippocampus in various modes of drug reinstatement behavior, the persisting effects of in vivo cocaine exposure on hippocampal synaptic plasticity are not sufficiently understood. In this report we investigated the effects of cocaine conditioning on long-term
- PMID 24464838
Japanese Journal
- Dynorphin A (1–13) Alleviated Stress-Induced Behavioral Impairments in Mice
- Mamiya Takayoshi,Hasegawa Yuya,Hiramatsu Masayuki
- Biological and Pharmaceutical Bulletin 37(8), 1269-1273, 2014
- … Dynorphin A (1–13) (1500 pmol/5 µL intracerebroventricular (i.c.v.)) attenuated the repeated stress-induced escape failures from the shock, and this improvement was inhibited by the pretreatment of nor-binaltorphimine (4.9 nmol/kg subcutaneously (s.c.)), a κ-opioid receptor antagonist. …
- NAID 130004677531
- Dynorphin-Kappa Opioid Receptor Signaling Partly Mediates Estrogen Negative Feedback Effect on LH Pulses in Female Rats
- MOSTARI Mst. Parvin,IEDA Nahoko,DEURA Chikaya [他],MINABE Shiori,YAMADA Shunji,UENOYAMA Yoshihisa,MAEDA Kei-ichiro,TSUKAMURA Hiroko
- The Journal of reproduction and development 59(3), 266-272, 2013-06-01
- … The effect of the injection of nor-binaltorphimine (nor-BNI), a kappa-opioid receptor (KOR) antagonist, into the third cerebroventricle (3V) on LH pulses was determined in ovariectomized (OVX) adult female rats with/without replacement of negative feedback levels of estradiol (low E2). … The mean LH concentrations and baseline levels of LH secretion in nor-BNI-injected, low E2-treated rats were significantly higher compared with vehicle-treated controls. …
- NAID 10031184756
- Occlusal Disharmony Transiently Impairs Learning and Memory in the Mouse by Increasing Dynorphin A Levels in the Amygdala
- YAMADA Kentaro,ONO Yumie,KUBO Kin-ya,YAMAMOTO Toshiharu,ONOZUKA Minoru
- Tohoku journal of experimental medicine 230(1), 49-57, 2013-05-01
- … However, the bite-raised mice treated with a dynorphin antagonist, nor-binaltorphimine, showed similar escape latency times to the times of sham-operated group, even on the 3rd day. …
- NAID 10031175419
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- A Search Service for Abbreviation / Long Form Abbreviation / Long Form : nor-BNI / nor-binaltorphimine
- View and buy high purity nor-Binaltorphimine dihydrochloride from Tocris Bioscience, the leading worldwide supplier of high performance life science reagents ... References Portoghese et al (1994) Structure-activity relationship of ...
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★リンクテーブル★
| リンク元 | 「norbinaltorphimine」「ノルビナルトルフィミン」 |
| 関連記事 | 「n」「NOR」「binaltorphimine」 |
「norbinaltorphimine」
「ノルビナルトルフィミン」
「n」
- n.
- pの前の[n]はmと記載する。synptom→symptom
「NOR」
- 核小体形成域 nucleolar organizer region