Details

Autor(en) / Beteiligte

• Wemmie, John A.
• Chen, Jianguo
• Askwith, Candice C.
• Hruska-Hageman, Alesia M.
• Price, Margaret P.
• Nolan, Brian C.
• Yoder, Patrick G.
• Lamani, Ejvis
• Hoshi, Toshinori
• Freeman, John H.
• Welsh, Michael J.

Titel

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

Ist Teil von

• Neuron (Cambridge, Mass.), 2002-04, Vol.34 (3), p.463-477

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2002

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.