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Effects of drinking water fluorosis on L-type calcium channel of hippocampal neurons in mice

机译:氟中毒对小鼠海马神经元L型钙通道的影响

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摘要

The study aimed to investigate the effects of drinking water fluorosis on L-type calcium channels (LTCCs) in mouse hippocampal neurons. A total of 60 newly weaned ICR male mice were randomly divided into control, low fluoride and high fluoride groups. After 3 and 6 months of exposure to fluoride, the patch clamp technique was used to detect the peak and relative values (I/lmax), steady-state activation curve ratio (G/Gmax), decay time constant, and tail current time constant of LTCCs currents in hippocampal CA1 region of mouse brain slices. Fluoride greatly reduced the serum and urinary calcium concentrations in mice, and the chronic fluorosis has a greater impact than subchronic fluorosis. The peak value of LTCCs current in pyramidal neurons of hippocampal CM area was significant and increased with the prolonged exposure time. The relative values of current and steady-state coefficients were changed greatly. The decay and tail current time increased significantly. High fluorine concentration indicates great peak value and open time of LTCCs opening. LTCCs are sensitive to fluoride exposure. The activation voltage of calcium channels induced by fluoride exposure is decreased, the opening time of calcium channels is prolonged, and the calcium influx per unit time increased, thereby overloading calcium concentration in neurons and this may be an explanation for intracellular calcium overload caused by fluoride. The imbalance of calcium metabolism caused by fluorosis may be a pathogenesis of brain injury induced by fluoride. Furthermore, the risk of brain damage from low-fluorine exposure cannot be ignored. (C) 2018 Elsevier Ltd. All rights reserved.
机译:该研究旨在调查氟中毒对小鼠海马神经元L型钙通道(LTCC)的影响。将60只新断奶的ICR雄性小鼠随机分为对照组,低氟和高氟组。暴露于氟化物3个月和6个月后,使用膜片钳技术检测峰和相对值(I / lmax),稳态活化曲线比(G / Gmax),衰减时间常数和尾电流时间常数小鼠脑切片海马CA1区LTCCs电流的变化。氟化物大大降低了小鼠的血清和尿钙浓度,慢性氟中毒的影响比慢性氟中毒更大。海马CM区锥体神经元的LTCCs电流峰值显着,并随着暴露时间的延长而增加。电流和稳态系数的相对值发生了很大变化。衰减和尾电流时间显着增加。高氟浓度表明LTCCs的峰值和打开时间很大。 LTCC对氟化物暴露敏感。氟化物暴露引起的钙通道激活电压降低,钙通道开放时间延长,每单位时间的钙流入增加,从而神经元中钙浓度超载,这可能是氟化物引起的细胞内钙超载的一种解释。氟中毒引起的钙代谢失衡可能是氟化物引起的脑损伤的发病机制。此外,不可忽视的是低氟暴露对大脑造成伤害的风险。 (C)2018 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Chemosphere 》 |2019年第4期| 169-175| 共7页
  • 作者单位

    Zhejiang Normal Univ, Coll Chem & Life Sci, Jinhua 321004, Peoples R China;

    Zhejiang Normal Univ, Coll Chem & Life Sci, Jinhua 321004, Peoples R China;

    Zhejiang Normal Univ, Coll Chem & Life Sci, Jinhua 321004, Peoples R China;

    Zhejiang Normal Univ, Coll Sports & Hlth Sci, Jinhua 321004, Zhejiang, Peoples R China;

    Zhejiang Normal Univ, Coll Xing Zhi, Jinhua 321004, Zhejiang, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Fluorosis; Calcium imbalance; Hippocampal CA1 region; LTCCs; Patch clamp;

    机译:氟中毒;钙失衡;海马CA1区;LTCCs;膜片钳;

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