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1
Effects of a monoclonal anti-acetylcholine receptor antibody on the avian end-plate.一种单克隆抗乙酰胆碱受体抗体对鸟类终板的作用。
J Physiol. 1989 Apr;411:271-83. doi: 10.1113/jphysiol.1989.sp017573.
2
Properties of end-plate channels in rats immunized against acetylcholine receptors.抗乙酰胆碱受体免疫大鼠终板通道的特性
J Physiol. 1981 Feb;311:251-66. doi: 10.1113/jphysiol.1981.sp013583.
3
Pre-and post-junctional effects of tubocurarine and other nicotinic antagonists during repetitive stimulation in the rat.筒箭毒碱及其他烟碱样拮抗剂在大鼠重复刺激过程中的接头前和接头后效应
J Physiol. 1984 Jun;351:275-97. doi: 10.1113/jphysiol.1984.sp015245.
4
Reaction of tetraethylammonium with the open and closed conformations of the acetylcholine receptor ionic channel complex.四乙铵与乙酰胆碱受体离子通道复合物的开放和关闭构象的反应。
J Gen Physiol. 1979 Jul;74(1):129-52. doi: 10.1085/jgp.74.1.129.
5
Interactions of bupivacaine with ionic channels of the nicotinic receptor. Electrophysiological and biochemical studies.布比卡因与烟碱样受体离子通道的相互作用。电生理学和生物化学研究。
Mol Pharmacol. 1984 Sep;26(2):293-303.
6
Neuromuscular Transmission in experimental autoimmune myasthenia gravis (EAMG). Quantitative ionophoresis and current fluctuation analysis at normal and myasthenic rat end-plates.实验性自身免疫性重症肌无力(EAMG)中的神经肌肉传递。正常和重症肌无力大鼠终板处的定量离子电渗疗法及电流波动分析。
Pflugers Arch. 1981 May;390(2):156-60. doi: 10.1007/BF00590199.
7
Meproadifen reaction with the ionic channel of the acetylcholine receptor: potentiation of agonist-induced desensitization at the frog neuromuscular junction.美普罗地芬与乙酰胆碱受体离子通道的反应:增强青蛙神经肌肉接头处激动剂诱导的脱敏作用。
Mol Pharmacol. 1982 Nov;22(3):636-47.
8
[End plate currents with a physiological level of quantal secretion and after potentiation of the mediator release by 4-aminopyridine].[具有量子分泌生理水平以及在4-氨基吡啶增强介质释放后的终板电流]
Neirofiziologiia. 1991;23(1):48-56.
9
End-plate currents evoked by paired stimuli in frog muscle fibres.青蛙肌肉纤维中由成对刺激诱发的终板电流。
Pflugers Arch. 1984 Jun;401(2):185-92. doi: 10.1007/BF00583880.
10
Effects of tubocurarine on end-plate current rundown and quantal content during rapid nerve stimulation in the snake.筒箭毒碱对蛇快速神经刺激期间终板电流衰减和量子含量的影响。
Clin Exp Pharmacol Physiol. 1988 Jun;15(6):479-90. doi: 10.1111/j.1440-1681.1988.tb01104.x.

引用本文的文献

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Effect of sera from seronegative myasthenia gravis patients on neuromuscular junctions.血清阴性重症肌无力患者血清对神经肌肉接头的影响。
Neurol Sci. 2013 Oct;34(10):1735-44. doi: 10.1007/s10072-013-1323-y. Epub 2013 Feb 7.
2
Active calcium accumulation underlies severe weakness in a panel of mice with slow-channel syndrome.主动钙蓄积是一组患有慢通道综合征小鼠严重肌无力的基础。
J Neurosci. 2002 Aug 1;22(15):6447-57. doi: 10.1523/JNEUROSCI.22-15-06447.2002.
3
Novel delta subunit mutation in slow-channel syndrome causes severe weakness by novel mechanisms.慢通道综合征中的新型δ亚基突变通过新机制导致严重肌无力。
Ann Neurol. 2002 Jan;51(1):102-12. doi: 10.1002/ana.10077.
4
Slow-channel transgenic mice: a model of postsynaptic organellar degeneration at the neuromuscular junction.慢通道转基因小鼠:神经肌肉接头处突触后细胞器退化的模型。
J Neurosci. 1997 Jun 1;17(11):4170-9. doi: 10.1523/JNEUROSCI.17-11-04170.1997.
5
Activation and blockade of mouse muscle nicotinic channels by antibodies directed against the binding site of the acetylcholine receptor.针对乙酰胆碱受体结合位点的抗体对小鼠肌肉烟碱型通道的激活和阻断作用
J Physiol. 1996 Apr 1;492 ( Pt 1)(Pt 1):107-14. doi: 10.1113/jphysiol.1996.sp021293.

本文引用的文献

1
Some properties of avian skeletal muscle fibres with multiple neuromuscular junctions.具有多个神经肌肉接头的鸟类骨骼肌纤维的一些特性。
J Physiol. 1960 Dec;154(3):581-98. doi: 10.1113/jphysiol.1960.sp006597.
2
A further study of the statistical composition on the end-plate potential.关于终板电位统计构成的进一步研究。
J Physiol. 1955 Oct 28;130(1):114-22. doi: 10.1113/jphysiol.1955.sp005397.
3
The effect of magnesium on the activity of motor nerve endings.镁对运动神经末梢活性的影响。
J Physiol. 1954 Jun 28;124(3):553-9. doi: 10.1113/jphysiol.1954.sp005128.
4
Monoclonal anti-acetylcholine-receptor antibodies directed against the cholinergic binding site.针对胆碱能结合位点的单克隆抗乙酰胆碱受体抗体。
Biochemistry. 1981 Sep 29;20(20):5920-4. doi: 10.1021/bi00523a041.
5
Functional activities of autoantibodies to acetylcholine receptors and the clinical severity of myasthenia gravis.抗乙酰胆碱受体自身抗体的功能活性与重症肌无力的临床严重程度
N Engl J Med. 1982 Sep 23;307(13):769-75. doi: 10.1056/NEJM198209233071301.
6
Monoclonal hybridoma anti-acetylcholine receptor antibodies: antibody specificity and effect of passive transfer.单克隆杂交瘤抗乙酰胆碱受体抗体:抗体特异性及被动转移的作用
Ann N Y Acad Sci. 1981;377:97-109. doi: 10.1111/j.1749-6632.1981.tb33726.x.
7
Anti-acetylcholine receptor antibodies directed against the alpha-bungarotoxin binding site induce a unique form of experimental myasthenia.针对α-银环蛇毒素结合位点的抗乙酰胆碱受体抗体可诱发一种独特形式的实验性肌无力。
Proc Natl Acad Sci U S A. 1983 Jul;80(13):4089-93. doi: 10.1073/pnas.80.13.4089.
8
Modification of alpha-bungarotoxin and cholinergic ligand-binding properties of Torpedo acetylcholine receptor by a monoclonal anti-acetylcholine receptor antibody.单克隆抗乙酰胆碱受体抗体对α-银环蛇毒素及电鳐乙酰胆碱受体胆碱能配体结合特性的修饰作用
J Biol Chem. 1984 Dec 25;259(24):15051-9.
9
Monoclonal antibodies modify acetylcholine-induced ionic channel properties in cultured chick myoballs.单克隆抗体可改变培养的鸡肌球中乙酰胆碱诱导的离子通道特性。
J Membr Biol. 1983;76(2):123-8. doi: 10.1007/BF02000612.
10
Properties of end-plate channels in rats immunized against acetylcholine receptors.抗乙酰胆碱受体免疫大鼠终板通道的特性
J Physiol. 1981 Feb;311:251-66. doi: 10.1113/jphysiol.1981.sp013583.

一种单克隆抗乙酰胆碱受体抗体对鸟类终板的作用。

Effects of a monoclonal anti-acetylcholine receptor antibody on the avian end-plate.

作者信息

Maselli R A, Nelson D J, Richman D P

机构信息

Department of Neurology, University of Chicago, IL 60637.

出版信息

J Physiol. 1989 Apr;411:271-83. doi: 10.1113/jphysiol.1989.sp017573.

DOI:10.1113/jphysiol.1989.sp017573
PMID:2614725
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190524/
Abstract
  1. The effects of anti-acetylcholine receptor (AChR) monoclonal antibodies (mAbs) 370 and 132A on miniature end-plate potentials (MEPPs) and end-plate currents (EPCs) in the posterior latissimus dorsi muscle of adult chickens were investigated. 2. After incubation of the electrophysiological preparation with mAb 370 (5-50 micrograms/ml), which blocks both agonist (carbamylcholine) and alpha-bungarotoxin (alpha-BTX) binding and induces a hyperacute form of experimental autoimmune myasthenia gravis (EAMG), MEPP and EPC amplitudes were irreversibly reduced. 3. This effect was not associated with any significant change in the time constant describing EPC decay (tau EPC), current reversal potential, or the voltage dependence of tau EPC. The tau EPC at -80 mV was 5.9 +/- 0.6 ms before incubation with mAb 370 (50 micrograms/ml) and 6.0 +/- 0.9 ms afterwards. Current reversal potential was -3.9 +/- 0.4 mV before mAb incubation and -4.8 +/- 1.5 mV afterwards. The change in membrane potential required to produce an e-fold change in tau EPC was 128 +/- 2.3 mV before antibody incubation compared to 125 +/- 6.6 mV after incubation. 4. A second anti-AChR mAb, 132A (50 micrograms/ml), which is capable of inducing the classically described form of EAMG without blocking agonist or alpha-BTX binding, or inducing hyperacute EAMG, produced no significant change in MEPP amplitude, EPC amplitude, tau EPC or EPC reversal potentials. 5. The mAb 370 (50 micrograms/ml) induced a partially reversible decrease of the quantal content of the neurally evoked end-plate potential (EPP). This effect was not observed with mAb 132A, (+)tubocurarine (10(-7)-10(-5) g/ml) or an irrelevant anti-oestrogen receptor mAb. 6. These data suggest that the rapid onset of weakness observed in chicken hatchlings after the injection of mAb 370 (Gomez & Richman, 1983) can be attributed to a combined effect of a block of acetylcholine (ACh)-induced ion channel activity in the postsynaptic membrane and a reduction of the neurally evoked release of acetylcholine from the nerve terminal.
摘要
  1. 研究了抗乙酰胆碱受体(AChR)单克隆抗体(mAb)370和132A对成年鸡背阔肌微小终板电位(MEPPs)和终板电流(EPCs)的影响。2. 用mAb 370(5 - 50微克/毫升)孵育电生理制剂后,该抗体可阻断激动剂(氨甲酰胆碱)和α-银环蛇毒素(α-BTX)的结合,并诱发超急性形式的实验性自身免疫性重症肌无力(EAMG),MEPP和EPC幅度不可逆地降低。3. 这种效应与描述EPC衰减的时间常数(tau EPC)、电流反转电位或tau EPC的电压依赖性的任何显著变化均无关。在与mAb 370(50微克/毫升)孵育前,-80 mV时的tau EPC为5.9±0.6毫秒,孵育后为6.0±0.9毫秒。mAb孵育前电流反转电位为-3.9±0.4 mV,孵育后为-4.8±1.5 mV。产生tau EPC e倍变化所需的膜电位变化在抗体孵育前为128±2.3 mV,孵育后为125±6.6 mV。4. 第二种抗AChR mAb,132A(50微克/毫升),能够诱发经典描述形式的EAMG,而不阻断激动剂或α-BTX结合,也不诱发超急性EAMG,对MEPP幅度、EPC幅度、tau EPC或EPC反转电位无显著影响。5. mAb 370(50微克/毫升)诱发神经诱发终板电位(EPP)量子含量部分可逆性降低。mAb 132A、(+)筒箭毒碱(10⁻⁷ - 10⁻⁵克/毫升)或无关的抗雌激素受体mAb未观察到这种效应。6. 这些数据表明,注射mAb 370后鸡雏中观察到的快速肌无力发作(Gomez和Richman,1983)可归因于突触后膜中乙酰胆碱(ACh)诱导的离子通道活性受阻以及神经末梢乙酰胆碱神经诱发释放减少的联合作用。