Acute effect of β amyloid on synchronized spontaneous Ca2+ oscillations in cultured hippocampal networks

Authors

  • Yanfang Rui,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Ruxin Li,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Yifu Liu,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Shaoqing Zhu,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Xinzhu Yu,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Zhonghua Sheng,

    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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  • Zuoping Xie

    Corresponding author
    1. Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China
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Corresponding author. Tel.: +86 10 62788677. zuopingx@mail.tsinghua.edu.cn

Abstract

The effects of β amyloid (Aβ) on cytoplasmic Ca2+ ([Ca2+]c) have been studied extensively, but the current literature on this aspect is confusing. We reported that 20 μM Aβ25–35 significantly inhibited the synchronized spontaneous cytoplasmic Ca2+ transients immediately after application, whereas it had little effect on the baseline [Ca2+]c concentration in neurons. Aβ1–42 had a similar effect on the Ca2+ transients as Aβ25–35, while it increased baseline [Ca2+]c concentration gradually. However, Aβ1–40 had little effect on either Ca2+ transients or baseline [Ca2+]c. Such differential effects of Aβ on Ca2+ signals might explain, at least partially, the confusing observations from the previous studies and provide important therapeutic implications for preventing or reversing early neuron damage in Alzheimer's disease.

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