Abstract
Acid-sensing ion channels (ASICs) activate following extracellular acidification that occurs physiologically in synaptic vesicle fusion or pathophysiologically during ischemia. Unsurprisingly, these trimeric cation channels have been shown to contribute to synaptic transmission and are important mediators of cell death during ischemia. In addition to the ionotropic function of ASIC1a, recent evidence suggests that ASIC1a metabotropically signals for cell death via the channel’s intracellular domains (ICDs).
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