{"title":"氯化亚锡增加小鼠运动神经末梢钙内流。","authors":"T Hattori, H Maehashi","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Stannous chloride (SnCl2) facilitates the calcium (Ca) entry into the frog motor nerve terminals. To compare the mode of action of SnCl2 on the Ca channels in the mouse with that in the frog, we investigated the effects of SnCl2 on the inward Ca current at the nerve terminals. SnCl2 (0.1 mM) did not change the second positive component of the action potential (an outward potassium (K) current) at the terminal part of the nerve terminal. SnCl2 (0.1 mM) increased the amplitude of the prolonged negative or positive deflection (an inward Ca current) evoked by treatment with 1 mM tetraethylammonium and 0.1 mM 3,4-diaminopyridine at the terminal or preterminal part of the nerve terminal, respectively. This augmenting effect of SnCl2 was inhibited by cumulative addition of Ca channel blockers, i.e., 0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2, or 10 mM MgCl2. From the results obtained, it has been confirmed that SnCl2 facilitates the transmitter release by enhancing the Ca influx at the nerve terminals but not by blocking the K channels and that the mode of action of SnCl2 in the mouse is identical with that in the frog.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 2","pages":"253-6"},"PeriodicalIF":0.0000,"publicationDate":"1994-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Augmentation of calcium influx by stannous chloride at mouse motor nerve terminals.\",\"authors\":\"T Hattori, H Maehashi\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Stannous chloride (SnCl2) facilitates the calcium (Ca) entry into the frog motor nerve terminals. To compare the mode of action of SnCl2 on the Ca channels in the mouse with that in the frog, we investigated the effects of SnCl2 on the inward Ca current at the nerve terminals. SnCl2 (0.1 mM) did not change the second positive component of the action potential (an outward potassium (K) current) at the terminal part of the nerve terminal. SnCl2 (0.1 mM) increased the amplitude of the prolonged negative or positive deflection (an inward Ca current) evoked by treatment with 1 mM tetraethylammonium and 0.1 mM 3,4-diaminopyridine at the terminal or preterminal part of the nerve terminal, respectively. This augmenting effect of SnCl2 was inhibited by cumulative addition of Ca channel blockers, i.e., 0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2, or 10 mM MgCl2. From the results obtained, it has been confirmed that SnCl2 facilitates the transmitter release by enhancing the Ca influx at the nerve terminals but not by blocking the K channels and that the mode of action of SnCl2 in the mouse is identical with that in the frog.</p>\",\"PeriodicalId\":21140,\"journal\":{\"name\":\"Research communications in chemical pathology and pharmacology\",\"volume\":\"84 2\",\"pages\":\"253-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1994-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Research communications in chemical pathology and pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research communications in chemical pathology and pharmacology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
氯化亚锡(SnCl2)促进钙(Ca)进入蛙运动神经末梢。为了比较SnCl2对小鼠和青蛙钙通道的作用方式,我们研究了SnCl2对神经末梢向内钙电流的影响。SnCl2 (0.1 mM)未改变神经末梢部动作电位的第二正分量(向外钾(K)电流)。SnCl2 (0.1 mM)分别增加了1 mM四乙基铵和0.1 mM 3,4-二氨基吡啶在神经末梢末端或前末端引起的长时间负或正偏转(向内Ca电流)的振幅。SnCl2的这种增强作用被Ca通道阻滞剂(即0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2或10 mM MgCl2)的累积添加抑制。结果表明,SnCl2通过增强神经末梢Ca内流而不是通过阻断K通道促进递质释放,并且SnCl2在小鼠中的作用方式与在青蛙中的作用方式相同。
Augmentation of calcium influx by stannous chloride at mouse motor nerve terminals.
Stannous chloride (SnCl2) facilitates the calcium (Ca) entry into the frog motor nerve terminals. To compare the mode of action of SnCl2 on the Ca channels in the mouse with that in the frog, we investigated the effects of SnCl2 on the inward Ca current at the nerve terminals. SnCl2 (0.1 mM) did not change the second positive component of the action potential (an outward potassium (K) current) at the terminal part of the nerve terminal. SnCl2 (0.1 mM) increased the amplitude of the prolonged negative or positive deflection (an inward Ca current) evoked by treatment with 1 mM tetraethylammonium and 0.1 mM 3,4-diaminopyridine at the terminal or preterminal part of the nerve terminal, respectively. This augmenting effect of SnCl2 was inhibited by cumulative addition of Ca channel blockers, i.e., 0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2, or 10 mM MgCl2. From the results obtained, it has been confirmed that SnCl2 facilitates the transmitter release by enhancing the Ca influx at the nerve terminals but not by blocking the K channels and that the mode of action of SnCl2 in the mouse is identical with that in the frog.