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The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory
John A Wemmie1, Jianguo Chen, Candice C Askwith
1Department of Psychiatry, University of Iowa, Iowa City, IA 52242, USA.
Neuron
|May 4, 2002
Summary
Acid-sensing ion channels (ASICs) are crucial for acid-activated currents in the brain. Loss of ASICs impairs synaptic plasticity, learning, and memory in mice.
Area of Science:
- Neuroscience
- Molecular Biology
- Physiology
Background:
- Central neurons exhibit significant acid-activated currents, but their molecular basis remains unidentified.
- Acid-sensing ion channels (ASICs) are implicated in neuronal function, but their specific role in the hippocampus is unclear.
Purpose of the Study:
- To identify the molecular identity of acid-activated currents in hippocampal neurons.
- To investigate the role of ASICs in synaptic transmission, plasticity, learning, and memory.
Main Methods:
- Utilized ASIC null mice to assess the impact of ASIC channel deletion on neuronal currents.
- Examined ASIC localization in hippocampal tissue, synaptosomes, and neuronal synapses.
- Measured excitatory postsynaptic potentials and NMDA receptor activation during high-frequency stimulation.
- Assessed spatial learning and eyeblink conditioning in ASIC null mice.
Main Results:
- Elimination of ASICs abolished H(+)-gated currents in hippocampal neurons.
- ASICs were found in the hippocampus, synaptosomes, and at synapses in dendrites.
- Loss of ASICs impaired hippocampal long-term potentiation and reduced excitatory postsynaptic potentials.
- ASIC null mice exhibited deficits in spatial learning and eyeblink conditioning.
Conclusions:
- ASICs are the primary molecular components responsible for acid-activated currents in hippocampal neurons.
- ASIC-mediated currents play a critical role in synaptic plasticity, learning, and memory processes.
- These findings highlight ASICs as potential therapeutic targets for cognitive disorders.