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

Abstract:

: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 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 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.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Liu MG,Li HS,Li WG,Wu YJ,Deng SN,Huang C,Maximyuk O,Sukach V,Krishtal O,Zhu MX,Xu TL

doi

10.1038/srep23350

subject

Has Abstract

pub_date

2016-03-21 00:00:00

pages

23350

issn

2045-2322

pii

srep23350

journal_volume

6

pub_type

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