Hippocampal neurons in direct contact with astrocytes exposed to amyloid β25-35 exhibit reduced excitatory synaptic transmission

Hippocampal neurons in direct contact with astrocytes exposed to amyloid β25-35 exhibit reduced excitatory synaptic transmission
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与暴露于淀粉样蛋白 β25-35 的星形胶质细胞直接接触的海马神经元表现出兴奋性突触传递减少

DOI:
10.1016/j.ibror.2019.07.1719
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发表时间:
2019
期刊:
影响因子:
2.6
通讯作者:
Katsunori Iwasaki
Katsunori Iwasaki
中科院分区:
--
文献类型:
--
作者:
Kohei Oyabu;Hiroki Kiyota;Kaori Kubota;Takuya Watanabe;Shutaro Katsurabayashi;Katsunori Iwasaki

文献摘要

相似文献

淀粉样β蛋白(Aβ)与阿尔茨海默病的进展密切相关,因为由Aβ组成的老年斑会引起突触抑制和突触异常。在中枢神经系统中,星形胶质细胞是一种主要的神经胶质细胞类型,其有助于调节突触传递和突触发生。在这项研究中,我们研究了星形胶质细胞暴露于Aβ片段25-35(Aβ25-35)是否影响突触传递。我们发现,海马神经元的突触传递受到暴露于Aβ25-35的星形胶质细胞的抑制。暴露于Aβ25-35的星形胶质细胞降低了兴奋性突触后释放和易于释放的突触池的大小。兴奋性突触的数量也减少。然而,兴奋性突触的数量没有变化,除非Aβ25-35暴露的星形胶质细胞和海马神经元之间有直接接触。这些数据表明,暴露于Aβ25-35的星形胶质细胞和神经元之间的直接接触对于抑制阿尔茨海默病进展中的突触传递至关重要。
Amyloid β protein (Aβ) is closely related to the progression of Alzheimer's disease because senile plaques consisting of Aβ cause synaptic depression and synaptic abnormalities. In the central nervous system, astrocytes are a major glial cell type that contribute to the modulation of synaptic transmission and synaptogenesis. In this study, we examined whether astrocytes exposed to Aβ fragment 25-35 (Aβ25-35) affect synaptic transmission. We show that synaptic transmission by hippocampal neurons was inhibited by astrocytes exposed to Aβ25-35. The Aβ25-35-exposed astrocytes lowered excitatory postsynaptic release and the size of the readily releasable synaptic pool. The number of excitatory synapses was also reduced. However, the number of excitatory synapses was unchanged unless there was direct contact between Aβ25-35-exposed astrocytes and hippocampal neurons. These data indicate that direct contact between Aβ25-35-exposed astrocytes and neurons is critical for inhibiting synaptic transmission in the progression of Alzheimer’s disease.