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期刊论文
The Acid-Activated Ion Channel ASIC Contributes to Synaptic Plasticity, Learning, and Memory
，-0001，（）：
Many central neurons possess large acid-activated inhibicurrents, 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 centransmission. Investigating this possibility, we found ASIC in hippocampus, in synaptosomes, and in den-drites localized at synapses. Moreover, loss of ASIC nerimpaired hippocampal long-term potentiation. ASIC null mice had reduced excitatory postsynaptic poten-tials and NMDA receptor activation during high-fre-quency stimulation. Consistent with these findings, null mice displayed defective spatial learning and eye-blink conditioning. These results identify ASIC as a key component of acid-activated currents and implicate these currents in processes underlying synaptic plas-ticity, learning, and memory.
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