Acid-sensing ion channel 1a contributes to hippocampal LTP inducibility through multiple mechanisms

• 作 者: Ming-Gang Liu Hu-Song Li Wei-Guang Li Yan-Jiao Wu Shi-Ning Deng Chen Huang Oleksandr Maximyuk Volodymyr Sukach Oleg Krishtal Michael X.Zhu Tian-LeXu
• 机 构: Discipline of Neuroscience and Department of Anatomy,Histology and Embryology,Collaborative Innovati
• 出 处: 第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
• 发表日期: 2016年3期
• 关键词: acid-sensing ion channel hippocampus long-term depression long-term potentiation

　　The exact roles of acid-sensing ion channels(ASICs)in synaptic plasticity remain elusive.Here,we address the contribution of ASIC1a to four types of synaptic plasticity in the mouse hippocampus using an in vitro multi-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 high frequency stimulation or theta burst stimulation in the CA1 region.ASIC1a has no role in hippocampal long-term depression induced by either low frequency stimulation or(RS)-3,5-dihydroxyphenylglycine.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 shed novel insights into the role of ASIC1a in hippocampal synaptic plasticity and the underlying mechanisms.Our unbiased study provides an objective way of assaying synaptic plasticity mechanisms in the brain.