PMID:11988176

Citation	Wemmie, JA, Chen, J, Askwith, CC, Hruska-Hageman, AM, Price, MP, Nolan, BC, Yoder, PG, Lamani, E, Hoshi, T, Freeman, JH Jr and Welsh, MJ (2002) The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory. Neuron 34:463-77
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.
Links	PubMed
Keywords	Animals; Conditioning, Eyelid; Excitatory Amino Acid Antagonists/pharmacology; Excitatory Postsynaptic Potentials; Hippocampus/cytology; Hippocampus/metabolism; Hydrogen-Ion Concentration; Kynurenic Acid/pharmacology; Learning/physiology; Long-Term Potentiation/physiology; Membrane Proteins; Memory/physiology; Mice; Mice, Knockout; Nerve Tissue Proteins/metabolism; Neuronal Plasticity/physiology; Neurons/drug effects; Neurons/metabolism; Patch-Clamp Techniques; Proteins/metabolism; Rats; Sodium Channels/genetics; Sodium Channels/metabolism; Synaptic Transmission/physiology
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.