Abstract
Acid‐sensing ion channel‐1a (ASIC1a) mediates H+‐gated current to influence normal brain physiology and impact several models of disease. Although ASIC2 subunits are widely expressed in brain and modulate ASIC1a current, their function remains poorly understood. We identified ASIC2a in dendrites, dendritic spines, and brain synaptosomomes. This localization depended on ASIC2a binding to PSD‐95 and matched that of ASIC1a, which does not bind PSD‐95. We found that ASIC2 and ASIC1a associated in brain, and through its interaction with PSD‐95, ASIC2 increased ASIC1a localization in dendritic spines. Loss of ASIC2 reduced the acid‐evoked elevation of [Ca2+]i in dendritic spines and impaired fear conditiong, both of which require ASIC1a. These results indicate that ASIC2 facilitates ASIC1a localization and function in dendritic spines and thereby fear‐related behavior.
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