| First Author | Wemmie JA | Year | 2002 |
| Journal | Neuron | Volume | 34 |
| Issue | 3 | Pages | 463-77 |
| PubMed ID | 11988176 | Mgi Jnum | J:76361 |
| Mgi Id | MGI:2179183 | Doi | 10.1016/s0896-6273(02)00661-x |
| Citation | Wemmie JA, et al. (2002) The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory. Neuron 34(3):463-77 |
| abstractText | 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. |
