兰伯特-伊顿综合征血清可降低钙电流：运动神经元受到优先影响，而L型电流未受影响。
Reduction of calcium currents by Lambert-Eaton syndrome sera: motoneurons are preferentially affected, and L-type currents are spared.
作者信息
García K D, Beam K G
机构信息
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523, USA.
出版信息
J Neurosci. 1996 Aug 15;16(16):4903-13. doi: 10.1523/JNEUROSCI.16-16-04903.1996.
Abstract
Previous work has demonstrated that Lambert-Eaton syndrome (LES) antibodies reduce calcium currents in nonneuronal cells and neurons and reduce the amplitude of extracellularly recorded currents at mouse motor nerve terminals. We compared effects of LES sera on whole-cell currents of cultured nerve and muscle. LES sera more strongly reduced calcium currents in motoneurons than in sensory neurons. Motoneuronal potassium currents were unaffected. The sera minimally affected calcium currents in skeletal and cardiac muscle. In motoneurons, both low voltage-activated (LVA) and high voltage-activated (HVA) components of calcium current were decreased, demonstrating that the sera targeted more than one calcium channel type. The HVA current remaining in LES-treated motoneurons was little affected by micromolar omega-conotoxin MVIIC but was reduced > 70% by micromolar nimodipine. This pharmacological profile contrasts with untreated cells and suggest that LES sera primarily spare L-type currents in motoneurons.
摘要
先前的研究表明，兰伯特-伊顿综合征（LES）抗体可降低非神经元细胞和神经元中的钙电流，并降低小鼠运动神经末梢细胞外记录电流的幅度。我们比较了LES血清对培养的神经细胞和肌肉细胞全细胞电流的影响。LES血清对运动神经元钙电流的降低作用比对感觉神经元更强。运动神经元的钾电流未受影响。这些血清对骨骼肌和心肌的钙电流影响极小。在运动神经元中，钙电流的低电压激活（LVA）成分和高电压激活（HVA）成分均降低，表明这些血清作用于不止一种钙通道类型。经LES处理的运动神经元中剩余的HVA电流受微摩尔浓度的ω-芋螺毒素MVIIC影响较小，但受微摩尔浓度的尼莫地平影响降低>70%。这种药理学特征与未处理的细胞不同，提示LES血清主要使运动神经元中的L型电流免受影响。
相似文献
1
Reduction of calcium currents by Lambert-Eaton syndrome sera: motoneurons are preferentially affected, and L-type currents are spared.兰伯特-伊顿综合征血清可降低钙电流：运动神经元受到优先影响，而L型电流未受影响。
J Neurosci. 1996 Aug 15;16(16):4903-13. doi: 10.1523/JNEUROSCI.16-16-04903.1996.
2
Passive transfer of Lambert-Eaton myasthenic syndrome induces dihydropyridine sensitivity of ICa in mouse motor nerve terminals.兰伯特-伊顿肌无力综合征的被动转移诱导小鼠运动神经末梢中ICa的二氢吡啶敏感性。
J Neurophysiol. 1998 Sep;80(3):1056-69. doi: 10.1152/jn.1998.80.3.1056.
3
Decreased calcium currents in motor nerve terminals of mice with Lambert-Eaton myasthenic syndrome.患有兰伯特-伊顿肌无力综合征的小鼠运动神经末梢钙电流降低。
J Physiol. 1995 Aug 15;487(1):115-23. doi: 10.1113/jphysiol.1995.sp020865.
4
Lambert-Eaton sera reduce low-voltage and high-voltage activated Ca2+ currents in murine dorsal root ganglion neurons.兰伯特-伊顿血清可降低小鼠背根神经节神经元中低电压和高电压激活的Ca2+电流。
Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9264-9. doi: 10.1073/pnas.93.17.9264.
5
Calcium channel subtypes in lamprey sensory and motor neurons.七鳃鳗感觉神经元和运动神经元中的钙通道亚型
J Neurophysiol. 1997 Sep;78(3):1334-40. doi: 10.1152/jn.1997.78.3.1334.
6
Specificity of omega-conotoxin MVIIC-binding and -blocking calcium channel antibodies in Lambert-Eaton myasthenic syndrome.兰伯特-伊顿肌无力综合征中ω-芋螺毒素MVIIC结合和阻断钙通道抗体的特异性
J Neurol. 1999 Jan;246(1):38-44. doi: 10.1007/s004150050303.
7
Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings.兰伯特-伊顿综合征抗体可抑制电鳐神经末梢中乙酰胆碱的释放及P/Q型钙离子通道。
J Physiol. 1998 Apr 15;508 ( Pt 2)(Pt 2):427-38. doi: 10.1111/j.1469-7793.1998.427bq.x.
8
Effect of Lambert-Eaton myasthenic syndrome antibodies on autonomic neurons in the mouse.兰伯特-伊顿肌无力综合征抗体对小鼠自主神经元的影响。
Ann Neurol. 1997 Aug;42(2):147-56. doi: 10.1002/ana.410420204.
9
Apamin-sensitive calcium-activated potassium currents (SK) are activated by persistent calcium currents in rat motoneurons.蜂毒明肽敏感的钙激活钾电流（SK）由大鼠运动神经元中的持续性钙电流激活。
J Neurophysiol. 2007 May;97(5):3314-30. doi: 10.1152/jn.01068.2006. Epub 2007 Mar 14.
10
Heterogeneity of calcium channel autoantibodies detected using a small-cell lung cancer line derived from a Lambert-Eaton myasthenic syndrome patient.使用源自一名兰伯特-伊顿肌无力综合征患者的小细胞肺癌细胞系检测到的钙通道自身抗体的异质性。
Neurology. 1994 Feb;44(2):334-8. doi: 10.1212/wnl.44.2.334.
引用本文的文献
1
Zebrafish as a Model System for the Study of Severe Ca2.1 (α) Channelopathies.斑马鱼作为研究严重Ca2.1（α）通道病的模型系统
Front Mol Neurosci. 2020 Feb 7;12:329. doi: 10.3389/fnmol.2019.00329. eCollection 2019.
2
A mutation in Ca2.1 linked to a severe neurodevelopmental disorder impairs channel gating.一种与严重神经发育障碍相关的 Ca2.1 突变会损害通道门控。
J Gen Physiol. 2019 Jun 3;151(6):850-859. doi: 10.1085/jgp.201812237. Epub 2019 Apr 23.
3
Tetanic depression is overcome by tonic adenosine A(2A) receptor facilitation of L-type Ca(2+) influx into rat motor nerve terminals.强直抑制可通过强直腺苷A(2A)受体促进L型Ca(2+)流入大鼠运动神经末梢来克服。
J Physiol. 2004 Oct 1;560(Pt 1):157-68. doi: 10.1113/jphysiol.2004.067595. Epub 2004 Aug 5.
4
Ca2+ channels as targets of neurological disease: Lambert-Eaton Syndrome and other Ca2+ channelopathies.作为神经疾病靶点的钙离子通道：兰伯特-伊顿综合征及其他钙离子通道病
J Bioenerg Biomembr. 2003 Dec;35(6):697-718. doi: 10.1023/b:jobb.0000008033.02320.10.
5
Passive transfer of Lambert-Eaton syndrome to mice induces dihydropyridine sensitivity of neuromuscular transmission.将兰伯特-伊顿综合征被动转移至小鼠会诱导神经肌肉传递的二氢吡啶敏感性。
J Physiol. 2002 Sep 1;543(Pt 2):567-76. doi: 10.1113/jphysiol.2002.021048.
6
Calcium channel subtypes contributing to acetylcholine release from normal, 4-aminopyridine-treated and myasthenic syndrome auto-antibodies-affected neuromuscular junctions.钙通道亚型对正常、经4-氨基吡啶处理以及受肌无力综合征自身抗体影响的神经肌肉接头处乙酰胆碱释放的作用。
Br J Pharmacol. 2002 Aug;136(8):1135-45. doi: 10.1038/sj.bjp.0704818.
7
Lambert-Eaton antibodies inhibit Ca2+ currents but paradoxically increase exocytosis during stimulus trains in bovine adrenal chromaffin cells.兰伯特-伊顿抗体抑制钙离子电流，但矛盾的是，在牛肾上腺嗜铬细胞的刺激串期间会增加胞吐作用。
J Neurosci. 1999 May 1;19(9):3384-95. doi: 10.1523/JNEUROSCI.19-09-03384.1999.
8
The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons.钠通道Scn8a是脊髓运动神经元钠电流密度出生后发育性增加的主要促成因素。
J Neurosci. 1998 Jul 15;18(14):5234-9. doi: 10.1523/JNEUROSCI.18-14-05234.1998.
9
Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings.兰伯特-伊顿综合征抗体可抑制电鳐神经末梢中乙酰胆碱的释放及P/Q型钙离子通道。
J Physiol. 1998 Apr 15;508 ( Pt 2)(Pt 2):427-38. doi: 10.1111/j.1469-7793.1998.427bq.x.
本文引用的文献
1
Electromyography and electric stimulation of nerves in diseases of motor unit; observations on myasthenic syndrome associated with malignant tumors.运动单位疾病中的肌电图和神经电刺激；对与恶性肿瘤相关的肌无力综合征的观察。
J Am Med Assoc. 1957 Mar 30;163(13):1117-24. doi: 10.1001/jama.1957.02970480021005.
2
Bronchial neoplasm with myasthenia; prolonged apnoea after administration of succinylcholine.支气管肿瘤伴重症肌无力；给予琥珀酰胆碱后出现长时间呼吸暂停。
Lancet. 1953 Dec 19;265(6799):1291-3. doi: 10.1016/s0140-6736(53)91358-0.
3
Lambert-Eaton sera reduce low-voltage and high-voltage activated Ca2+ currents in murine dorsal root ganglion neurons.兰伯特-伊顿血清可降低小鼠背根神经节神经元中低电压和高电压激活的Ca2+电流。
Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9264-9. doi: 10.1073/pnas.93.17.9264.
4
Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release.多种钙离子通道类型共同存在以调节突触体神经递质释放。
Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9518-22. doi: 10.1073/pnas.90.20.9518.
5
Inhibitory action of Lambert-Eaton syndrome IgG on calcium currents in a thyroid C-cell line.兰伯特-伊顿综合征IgG对甲状腺C细胞系钙电流的抑制作用。
Ann N Y Acad Sci. 1993 Jun 21;681:398-401. doi: 10.1111/j.1749-6632.1993.tb22919.x.
6
Lambert-Eaton syndrome IgG inhibits dihydropyridine-sensitive, slowly inactivating calcium channels in bovine adrenal chromaffin cells.兰伯特-伊顿综合征免疫球蛋白G抑制牛肾上腺嗜铬细胞中对二氢吡啶敏感、缓慢失活的钙通道。
Ann N Y Acad Sci. 1993 Jun 21;681:394-7. doi: 10.1111/j.1749-6632.1993.tb22918.x.
7
Primary structure and functional expression of the omega-conotoxin-sensitive N-type calcium channel from rabbit brain.兔脑ω-芋螺毒素敏感型N型钙通道的一级结构与功能表达
Neuron. 1993 Apr;10(4):585-98. doi: 10.1016/0896-6273(93)90162-k.
8
Heterogeneity of calcium channel autoantibodies detected using a small-cell lung cancer line derived from a Lambert-Eaton myasthenic syndrome patient.使用源自一名兰伯特-伊顿肌无力综合征患者的小细胞肺癌细胞系检测到的钙通道自身抗体的异质性。
Neurology. 1994 Feb;44(2):334-8. doi: 10.1212/wnl.44.2.334.
9
Synaptotagmin can cause an immune-mediated model of Lambert-Eaton myasthenic syndrome in rats.突触结合蛋白可在大鼠中引发兰伯特-伊顿肌无力综合征的免疫介导模型。
Ann Neurol. 1994 Jan;35(1):74-80. doi: 10.1002/ana.410350112.
10
Adenosine acting at an A1 receptor decreases N-type calcium current in mouse motoneurons.作用于A1受体的腺苷可降低小鼠运动神经元中的N型钙电流。
J Neurosci. 1994 Jun;14(6):3628-34. doi: 10.1523/JNEUROSCI.14-06-03628.1994.
Zotero 插件