Involvement of intracellular Zn2+ signaling in LTP at perforant pathway-CA1 pyramidal cell synapse.
Involvement of intracellular Zn2+ signaling in LTP at perforant pathway-CA1 pyramidal cell synapse.
复制标题
细胞内 Zn2 信号传导参与穿通通路 - CA1 锥体细胞突触的 LTP。
DOI：
10.1002/hipo.22730
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发表时间：
2017
期刊：
影响因子：
3.5
通讯作者：
Atsushi Takeda
中科院分区：
文献类型：
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作者：
Haruna Tamano;Ryusuke Nishio;Atsushi Takeda
研究了穿孔通路- ca1锥体细胞突触中Zn2+信号通路的生理意义。使用连接微透析探针的记录电极诱导穿孔通路- ca1锥体细胞突触的体内长期增强（LTP），并通过微透析探针向记录区域局部灌注人工脑脊液（ACSF）。穿孔通路LTP在细胞外Zn2+螯合剂CaEDTA （10 mM）的灌注下没有减弱，但在细胞内Zn2+螯合剂ZnAF‐2DA （50 μM）的灌注下减弱，这表明细胞内Zn2+信号是穿孔通路LTP的必要条件。即使在ACSF中浸泡了CaEDTA的大鼠脑切片中，用细胞内ZnAF‐2测量的细胞内Zn2+水平，在穿孔通路- ca1锥体细胞突触所在的空洞层分子中，在强电刺激后也增加了。这些结果表明，细胞内起源于内部储存/蛋白质的Zn2+信号通路参与了穿孔通路- ca1锥体细胞突触的LTP。由于源于突触前Zn2+释放的细胞外Zn2+流入参与了Schaffer侧枝- CA1锥体细胞突触的LTP，突触依赖的Zn2+动力学可能参与了突触后CA1锥体细胞的可塑性。
Physiological significance of synaptic Zn2+signaling was examined at perforant pathway–CA1 pyramidal cell synapses.In vivolong‐term potentiation (LTP) at perforant pathway–CA1 pyramidal cell synapses was induced using a recording electrode attached to a microdialysis probe and the recording region was locally perfused with artificial cerebrospinal fluid (ACSF) via the microdialysis probe. Perforant pathway LTP was not attenuated under perfusion with CaEDTA (10 mM), an extracellular Zn2+chelator, but attenuated under perfusion with ZnAF‐2DA (50 μM), an intracellular Zn2+chelator, suggesting that intracellular Zn2+signaling is required for perforant pathway LTP. Even in rat brain slices bathed in CaEDTA in ACSF, intracellular Zn2+level, which was measured with intracellular ZnAF‐2, was increased in the stratum lacunosum‐moleculare where perforant pathway–CA1 pyramidal cell synapses were contained after tetanic stimulation. These results suggest that intracellular Zn2+signaling, which originates in internal stores/proteins, is involved in LTP at perforant pathway–CA1 pyramidal cell synapses. Because the influx of extracellular Zn2+, which originates in presynaptic Zn2+release, is involved in LTP at Schaffer collateral‐CA1 pyramidal cell synapses, synapse‐dependent Zn2+dynamics may be involved in plasticity of postsynaptic CA1 pyramidal cells.