Acid-sensing ion channel 1a contributes to hippocampal LTP inducibility through multiple mechanisms.
Acid-sensing ion channel 1a contributes to hippocampal LTP inducibility through multiple mechanisms.
复制标题
酸敏感离子通道 1a 通过多种机制促进海马 LTP 诱导
DOI：
10.1038/srep23350
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发表时间：
2016-03-21
影响因子：
4.6
通讯作者：
Xu TL
中科院分区：
文献类型：
--
作者：
Liu MG;Li HS;Li WG;Wu YJ;Deng SN;Huang C;Maximyuk O;Sukach V;Krishtal O;Zhu MX;Xu TL
酸敏感离子通道(ASIC)在突触可塑性中的确切作用仍不清楚。在这里，我们使用体外多电极阵列记录系统，研究ASIC1a在小鼠海马区五种形式突触可塑性中的作用。我们发现，ASIC1a的基因缺失或药物阻断大大减少了CA1区由单一或重复高频刺激或theta Burst刺激诱导的长时程增强(LTP)的可能性，但并未完全消除。然而，这些治疗并不影响低频电刺激或(RS)-3，5-二羟基苯甘氨酸引起的海马区长期抑郁。我们还表明，ASIC1a通过多种机制在海马LTP中发挥作用，包括但不限于增强NMDA受体功能。综上所述，这些结果揭示了ASIC1a在海马区突触可塑性中的作用及其潜在机制。这项不偏不倚的研究还展示了一种新的客观方法来分析大脑中的突触可塑性机制。
The exact roles of acid-sensing ion channels (ASICs) in synaptic plasticity remain elusive. Here, we address the contribution of ASIC1a to five forms of synaptic plasticity in the mouse hippocampus using anin vitromulti-electrode array recording system. We found that genetic deletion or pharmacological blockade of ASIC1a greatly reduced, but did not fully abolish, the probability of long-term potentiation (LTP) induction by either single or repeated high frequency stimulation or theta burst stimulation in the CA1 region. However, these treatments did not affect hippocampal long-term depression induced by low frequency electrical stimulation or (RS)-3,5-dihydroxyphenylglycine. We also show that ASIC1a exerts its action in hippocampal LTP through multiple mechanisms that include but are not limited to augmentation of NMDA receptor function. Taken together, these results reveal new insights into the role of ASIC1a in hippocampal synaptic plasticity and the underlying mechanisms. This unbiased study also demonstrates a novel and objective way to assay synaptic plasticity mechanisms in the brain.