钙对电突触的解偶联作用。
Uncoupling of electrotonic synapses by calcium.
作者信息
Baux G, Simonneau M, Tauc L, Segundo J P
出版信息
Proc Natl Acad Sci U S A. 1978 Sep;75(9):4577-81. doi: 10.1073/pnas.75.9.4577.
Abstract
The degree of axo-axonal synaptic coupling between nerve cells in the buccal ganglion of Navanax was investigated in relation to intracellular ionic calcium. Increasing intracellular Ca2+ by injection of Ca2+, injection of Na+, or application of ionophore X537A produced uncoupling after at least 90 min, if metabolic inhibitor was present in the medium. Subsequent removal of the metabolic inhibitor reestablished the coupling in less than 30 min. Injected Sr2+ also mimicked the uncoupling action of Ca2+. The presence of a metabolic inhibitor alone had no effect on the coupling. These results lead to the following conclusions: (i) Uncoupling is due to an increased free Ca2+ concentration at the junctions. (ii) The liberation of endogenous sequestered Ca2+ is not sufficient to produce uncoupling except if an excess Ca2+ had been previously sequestered. The electrical synapses in the buccal ganglion of Navanax thus appear to be affected by Ca2+ in a similar way as gap junctions studied in non-neural tissues.
摘要
研究了纳氏海蜗牛颊神经节中神经细胞之间轴突-轴突突触耦合程度与细胞内离子钙的关系。如果培养基中存在代谢抑制剂，通过注射Ca²⁺、注射Na⁺或应用离子载体X537A来增加细胞内Ca²⁺，至少90分钟后会导致解偶联。随后去除代谢抑制剂可在不到30分钟内重新建立耦合。注射Sr²⁺也模拟了Ca²⁺的解偶联作用。单独存在代谢抑制剂对耦合没有影响。这些结果得出以下结论：（i）解偶联是由于连接处游离Ca²⁺浓度增加。（ii）内源性螯合Ca²⁺的释放不足以产生解偶联，除非先前已经螯合了过量的Ca²⁺。因此，纳氏海蜗牛颊神经节中的电突触似乎与在非神经组织中研究的间隙连接一样，受到Ca²⁺的类似影响。
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