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醋酸铊对小鼠神经肌肉接头处阶段性递质释放的作用。

The action of thallium acetate on phasic transmitter release in the mouse neuromuscular junction.

作者信息

Wiegand H, Lohmann H, Chandra S V

出版信息

Arch Toxicol. 1986 Apr;58(4):265-70. doi: 10.1007/BF00297118.

DOI:10.1007/BF00297118
PMID:2424403
Abstract

Endplate potentials (EPP's) and miniature endplate potentials (MEPP's) were recorded from neuromuscular junctions of the mouse phrenic nerve-diaphragm preparation, blocked by high Mg++ (12 X 10(-3) mol/l)-Ringer. Superfusion of the preparations with Mg++-Ringer solutions containing thallium acetate (5 X 10(-4) mol/l Tlac) decreased phasic transmitter release as judged by EPP amplitudes as well as average quantal content, until total synaptic blockade (within about 300 min) occurred. Simultaneously MEPP amplitudes remained unchanged, whereas the frequency of MEPP's increased. When EPP amplitudes and/or quantal content were reduced by 50% (usually within about 180 min), superfusion with Mg++-Ringer solution without Tlac did not restore phasic transmitter release. However, the increase in spontaneous transmitter release was reversible, as MEPP frequencies returned to normal values. 4-Aminopyridine (5 X 10(-4) mol/l 4-AP) as added to the bath solution in the state of 50%-reduced phasic release temporarily restored EPP amplitudes and average quantal content, whereas MEPP amplitudes remained unchanged. It is concluded that thallium irreversibly blocks phasic transmitter release, whereas spontaneous transmitter release is reversibly enhanced.

摘要

在高镁(12×10⁻³mol/L)-林格液阻断的小鼠膈神经-膈肌标本的神经肌肉接头处记录终板电位(EPP)和微小终板电位(MEPP)。用含醋酸铊(5×10⁻⁴mol/L Tlac)的镁-林格液灌流标本,根据EPP幅度和平均量子含量判断,相性递质释放减少,直至完全突触阻断(约300分钟内)发生。同时,MEPP幅度保持不变,而MEPP的频率增加。当EPP幅度和/或量子含量降低50%(通常在约180分钟内)时,用不含Tlac的镁-林格液灌流不能恢复相性递质释放。然而,自发递质释放的增加是可逆的,因为MEPP频率恢复到正常值。在相性释放减少50%的状态下,向浴液中加入4-氨基吡啶(5×10⁻⁴mol/L 4-AP)可暂时恢复EPP幅度和平均量子含量,而MEPP幅度保持不变。结论是铊不可逆地阻断相性递质释放,而自发递质释放则可逆性增强。

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本文引用的文献

1
4-Aminopyridine does not increase m.e.p.p. frequencies at junctions depolarized by potassium.4-氨基吡啶不会增加由钾离子去极化的接头处微小终板电位的频率。
Brain Res. 1981 Apr 6;210(1-2):467-70. doi: 10.1016/0006-8993(81)90928-8.
2
The action of thallium acetate on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation.醋酸铊对大鼠膈神经 - 膈肌标本神经肌肉传递的作用。
Arch Toxicol. 1984 Mar;55(1):55-8. doi: 10.1007/BF00316586.
3
Influence of heavy metals on synaptic transmission: a review.重金属对突触传递的影响:综述
Neurotoxicology. 1983 Winter;4(4):69-83.
4
Lead and other metals can substitute for Ca2+ in calmodulin.铅和其他金属可以在钙调蛋白中替代钙离子(Ca2+)。
Arch Toxicol. 1983 Sep;54(1):61-70. doi: 10.1007/BF00277816.
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Presynaptic currents in mouse motor endings.小鼠运动终末的突触前电流。
J Physiol. 1982 Dec;333:619-36. doi: 10.1113/jphysiol.1982.sp014472.
6
Aminopyridines and synaptic transmission.氨基吡啶与突触传递
Neuroscience. 1980;5(8):1413-9. doi: 10.1016/0306-4522(80)90002-0.
7
Increase in transmitter release from motor nerve terminals induced by some pyridine derivatives.某些吡啶衍生物引起运动神经末梢递质释放增加。
Acta Physiol Pharmacol Latinoam. 1984;34(4):409-18.
8
The action of thallium acetate on spontaneous transmitter release in the rat neuromuscular junction.醋酸铊对大鼠神经肌肉接头处自发性递质释放的作用。
Arch Toxicol. 1984 Oct;55(4):253-7. doi: 10.1007/BF00341021.
9
Transmitter release in tetanus and botulinum A toxin-poisoned mammalian motor endplates and its dependence on nerve stimulation and temperature.破伤风毒素和肉毒杆菌A毒素中毒的哺乳动物运动终板中的递质释放及其对神经刺激和温度的依赖性。
Pflugers Arch. 1983 Nov;399(3):228-34. doi: 10.1007/BF00656720.
10
The calmodulin hypothesis of neurotransmission.神经传递的钙调蛋白假说。
Cell Calcium. 1981 Aug;2(4):365-85. doi: 10.1016/0143-4160(81)90026-9.