Journal
NEURON
Volume 34, Issue 3, Pages 463-477Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(02)00661-X
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Funding
- NHLBI NIH HHS [HL 64645, HL 14338] Funding Source: Medline
- NIDDK NIH HHS [DK 25295] Funding Source: Medline
- NIGMS NIH HHS [GM 57654] Funding Source: Medline
- NINDS NIH HHS [NS 38890] Funding Source: Medline
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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 eye-blink 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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