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The Acid-Activated Ion Channel ASIC Contributes to Synaptic Plasticity, Learning, and Memory
Journal article   Open access   Peer reviewed

The Acid-Activated Ion Channel ASIC Contributes to Synaptic Plasticity, Learning, and Memory

John A Wemmie, Jianguo Chen, Candice C Askwith, Alesia M Hruska-Hageman, Margaret P Price, Brian C Nolan, Patrick G Yoder, Ejvis Lamani, Toshinori Hoshi, John H Freeman, …
Neuron (Cambridge, Mass.), Vol.34(3), pp.463-477
2002
DOI: 10.1016/S0896-6273(02)00661-X
PMID: 11988176
url
https://doi.org/10.1016/S0896-6273(02)00661-XView
Published (Version of record) Open Access

Abstract

Many central neurons possess large acid-activated currents, yet their molecular identity is unknown. We found that eliminating the acid sensing ion channel (ASIC) abolished H +-gated currents in hippocampal neurons. Neuronal H +-gated currents and transient acidification are proposed to play a role in synaptic transmission. Investigating this possibility, we found ASIC in hippocampus, in synaptosomes, and in dendrites localized at synapses. Moreover, loss of ASIC impaired hippocampal long-term potentiation. ASIC null mice had reduced excitatory postsynaptic potentials and NMDA receptor activation during high-frequency stimulation. Consistent with these findings, null mice displayed defective spatial learning and eyeblink conditioning. These results identify ASIC as a key component of acid-activated currents and implicate these currents in processes underlying synaptic plasticity, learning, and memory.

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