抗コリン薬
WordNet
- a substance that opposes or blocks the action of acetylcholine (同)anticholinergic_drug
- inhibiting or blocking the action of acetylcholine at a receptor site; "anticholinergic drugs"
- a drug that neutralizes or counteracts the effects of another drug
- a muscle that relaxes while another contracts; "when bending the elbow the triceps are the antagonist"
- releasing or activated by acetylcholine or a related compound
PrepTutorEJDIC
- 対立する人,敵対者,競争相手(opponent)
UpToDate Contents
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English Journal
- Neurotransmissions of antidepressant-like effects of neuromedin U-23 in mice.
- Tanaka M1, Telegdy G2.Author information 1Department of Pathophysiology, MTA-SZTE Neuroscience Research Group, Faculty of Medicine, University of Szeged, Semmelweis 1, 6701 Szeged, Hungary.2Department of Pathophysiology, MTA-SZTE Neuroscience Research Group, Faculty of Medicine, University of Szeged, Semmelweis 1, 6701 Szeged, Hungary. Electronic address: telegdy@patph.szote.u-szeged.hu.AbstractNeuromedin U (NmU) is a widely distributed and multifunctional peptide in the central nervous system and the peripheral tissues. Little is know about the mechanisms of NmU on brain functions. The rodent isoform of the NmU, NmU-23, has been shown to have anxiolytic effects involved in the β-adrenergic and cholinergic nervous systems in elevated plus maze test. NmU-23 was tested for antidepressant-like effects in modified forced swimming test (FST) in mice and furthermore, the involvement of the adrenergic, serotonergic, cholinergic, dopaminergic or gaba-ergic receptors in the antidepressant-like effect of NmU-23 was studied in modified mice FST. Mice were pretreated with a non-selective α-adrenergic receptor antagonist phenoxybenzamine, an α1/α2β-adrenergic receptor antagonist, prazosin, an α2-adrenergic receptor antagonist, yohimbine, a β-adrenergic receptor antagonist, propranolol, a mixed 5-HT1/5-HT2 serotonergic receptor antagonist, methysergide, a non-selective 5-HT2 serotonergic receptor antagonist, cyproheptadine, nonselective muscarinic acetylcholine receptor antagonist, atropine, D2,D3,D4 dopamine receptor antagonist, haloperidol or γ-aminobutyric acid subunit A (GABAA) receptor antagonist, bicuculline. NmU-23 showed the antidepressant-like effects by decreasing the immobility time and increasing the climbing and swimming time. Prazosin, haloperidol, and bicuculline prevented the effects of NmU-23 on the climbing and swimming time. Methysergide and cyproheptadine prevented the effects of NmU-23 on the immobility, swimming and climbing time. Atropine prevented the effects of NmU-23 on the climbing time. Phenoxybenzamine, yohimbine and propranolol did not change the effects of NmU-23. The results demonstrated that the antidepressant-like effect of NmU-23 is mediated, at least in part, by an interaction of the α2-adrenergic, 5-HT1-2 serotonergic, D2,D3,D4 dopamine receptor, muscarinic acetylcholine receptors and γ-aminobutyric acid subunit A (GABAA) receptor in a modified mouse FST.
- Behavioural brain research.Behav Brain Res.2014 Feb 1;259:196-9. doi: 10.1016/j.bbr.2013.11.005. Epub 2013 Nov 13.
- Neuromedin U (NmU) is a widely distributed and multifunctional peptide in the central nervous system and the peripheral tissues. Little is know about the mechanisms of NmU on brain functions. The rodent isoform of the NmU, NmU-23, has been shown to have anxiolytic effects involved in the β-adrenerg
- PMID 24239690
- Behavioral disturbances in adult mice following neonatal virus infection or kynurenine treatment - Role of brain kynurenic acid.
- Liu XC1, Holtze M1, Powell SB2, Terrando N1, Larsson MK1, Persson A1, Olsson SK1, Orhan F1, Kegel M1, Asp L3, Goiny M1, Schwieler L1, Engberg G1, Karlsson H3, Erhardt S4.Author information 1Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.2Department of Psychiatry, University of California San Diego, La Jolla, CA, USA.3Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.4Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. Electronic address: sophie.erhardt@ki.se.AbstractExposure to infections in early life is considered a risk-factor for developing schizophrenia. Recently we reported that a neonatal CNS infection with influenza A virus in mice resulted in a transient induction of the brain kynurenine pathway, and subsequent behavioral disturbances in immune-deficient adult mice. The aim of the present study was to investigate a potential role in this regard of kynurenic acid (KYNA), an endogenous antagonist at the glycine site of the N-methyl-d-aspartic acid (NMDA) receptor and at the cholinergic α7 nicotinic receptor. C57BL/6 mice were injected i.p. with neurotropic influenza A/WSN/33 virus (2400 plaque-forming units) at postnatal day (P) 3 or with l-kynurenine (2×200mg/kg/day) at P7-16. In mice neonatally treated with l-kynurenine prepulse inhibition of the acoustic startle, anxiety, and learning and memory were also assessed. Neonatally infected mice showed enhanced sensitivity to d-amphetamine-induced (5mg/kg i.p.) increase in locomotor activity as adults. Neonatally l-kynurenine treated mice showed enhanced sensitivity to d-amphetamine-induced (5mg/kg i.p.) increase in locomotor activity as well as mild impairments in prepulse inhibition and memory. Also, d-amphetamine tended to potentiate dopamine release in the striatum in kynurenine-treated mice. These long-lasting behavioral and neurochemical alterations suggest that the kynurenine pathway can link early-life infection with the development of neuropsychiatric disturbances in adulthood.
- Brain, behavior, and immunity.Brain Behav Immun.2014 Feb;36:80-9. doi: 10.1016/j.bbi.2013.10.010. Epub 2013 Oct 17.
- Exposure to infections in early life is considered a risk-factor for developing schizophrenia. Recently we reported that a neonatal CNS infection with influenza A virus in mice resulted in a transient induction of the brain kynurenine pathway, and subsequent behavioral disturbances in immune-deficie
- PMID 24140727
- Tiotropium sustains the anti-inflammatory action of olodaterol via the cyclic AMP pathway.
- Costa L1, Roth M2, Miglino N1, Keglowich L1, Zhong J1, Lardinois D3, Tamm M2, Borger P4.Author information 1Pulmonary Cell Research, Department of Biomedicine, University Hospital Basel, Switzerland.2Pulmonology, Department of Internal medicine, University Hospital Basel, Switzerland.3Department of Thoracic Surgery, University Hospital Basel, CH-4031 Basel, Switzerland.4Pulmonary Cell Research, Department of Biomedicine, University Hospital Basel, Switzerland. Electronic address: pieter.borger@unibas.ch.AbstractMesenchymal cells (fibroblasts) of the airway wall respond to cholinergic stimulation by releasing pro-inflammatory and chemotactic cytokines and may thus contribute to chronic inflammation of the lung. Here, we studied the anti-inflammatory potential of olodaterol, a long acting β2-adrenergic receptor agonist, and tiotropium, a long-acting muscarinic receptor antagonist, and whether they interact at the level of the cyclic AMP dependent signaling pathway. Pulmonary fibroblasts of asthmatic (n = 9) and non-asthmatic (n = 8) subjects were stimulated with the muscarinic receptor agonist carbachol and interleukin-1β (IL-1 beta) in presence or absence of tiotropium or olodaterol alone, or their combination. We also measured cAMP levels and phosphorylation of the cAMP response element binding protein (CREB). As single components, carbachol, olodaterol and tiotropium did not affect IL-6 and IL-8 release. Carbachol concentration-dependently enhanced the production of IL-1β-induced IL-6 and IL-8, which was blocked by the simultaneous addition of tiotropium. The combination of olodaterol plus tiotropium further reduced IL-6 and IL-8 release. Olodaterol induced cAMP and the phosphorylation of CREB, an effect counteracted by carbachol, but rescued by tiotropium. We conclude that olodaterol plus tiotropium cooperate to decrease the inflammatory response in pulmonary fibroblasts in vitro.
- Pulmonary pharmacology & therapeutics.Pulm Pharmacol Ther.2014 Feb;27(1):29-37. doi: 10.1016/j.pupt.2013.11.001. Epub 2013 Nov 19.
- Mesenchymal cells (fibroblasts) of the airway wall respond to cholinergic stimulation by releasing pro-inflammatory and chemotactic cytokines and may thus contribute to chronic inflammation of the lung. Here, we studied the anti-inflammatory potential of olodaterol, a long acting β2-adrenergic rece
- PMID 24269928
Japanese Journal
- Nicotinic Acetylcholine Receptors Mediate the Suppressive Effect of an Injection of Diluted Bee Venom into the GV3 Acupoint on Oxaliplatin-Induced Neuropathic Cold Allodynia in Rats
- 認知症の予防・治療技術開発の新しい戦略<br/>—天然物を用いたアプローチ—
- Nicotinic acetylcholine receptors mediate the suppressive effect of an injection of diluted bee venom into the GV3 acupoint on oxaliplatin-induced neuropathic cold allodynia in rats
Related Links
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Related Pictures
★リンクテーブル★
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- 英
- anticholinergics, anticholinergic, anticholinergic agent, anticholinergic drug anticholinergic drugs, cholinolytic, cholinolytic drug, cholinergic antagonist
- 同
- 抗コリン剤、抗コリン作用薬、コリン作用遮断薬 cholinergic blocking agent
- 関
- ムスカリン性受容体拮抗薬 muscarinic antagonist。副交感神経遮断薬
- 副交感神経ムスカリン受容体拮抗薬であり、副交感神経作用を抑制する。
抗コリン薬の主な作用
- (YN2010 抗コリン薬(神経精神))
- 1. 散瞳作用:眼底検査や虹彩炎治療など
- 2. 膀胱利尿筋弛緩作用:尿路結石症鎮痙
- 3. 腺分泌抑制作用:麻酔前投与
- 4. 胃酸分泌抑制作用:抗胃潰瘍
- 5. 消化管運動抑制作用
- 6. 抗Parkinson作用
- 7. 抗迷走神経作用:徐脈性不整脈の治療
- 8. 農薬解毒作用:有機リン剤、カーバメート剤の解毒
therapeutic uses of muscarinic receptor antagonists
- GOO.195
- 呼吸器:気道分泌抑制。(アトロピンは気道分泌を抑制し、分泌物が乾固しうるが、イプラトロピウム、チオトロピウムはmucociliary clearanceにおける副作用を呈しないので、気道疾患に用いられている)
- 泌尿器:過活動性膀胱、夜尿症、対麻痺における頻尿
- 消化器:抗潰瘍薬(M1受容体選択性のある薬剤。ピレンゼピン、テレンゼピン)。鎮痙薬
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- 関
- anticholinergic、anticholinergic agent、anticholinergic drug、anticholinergics、cholinergic antagonist、cholinolytic、cholinolytic drug、muscarinic receptor antagonist
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- 関
- anticholinergic agent、anticholinergic drug、anticholinergics、cholinergic antagonist、cholinolytic、cholinolytic drug、muscarinic antagonist
[★]
- 関
- anticholinergic、anticholinergic agent、anticholinergic drug、anticholinergics、cholinergic antagonist、cholinolytic drug、muscarinic antagonist
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