The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory

Academic Article

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.
  • Authors

    Published In

  • Neuron  Journal
  • Digital Object Identifier (doi)

    Author List

  • Wemmie JA; Chen J; Askwith CC; Hruska-Hageman AM; Price MP; Nolan BC; Yoder PG; Lamani E; Hoshi T; Freeman JH
  • Start Page

  • 463
  • End Page

  • 477
  • Volume

  • 34
  • Issue

  • 3