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ASIC1a is a proton-gated Na + and Ca 2+ ion channel that can be activated in response to acidic pH (Yermolaieva et al., 2004), and it has been shown to participate in seizure termination by activating hippocampal inhibitory interneurons, which exhibited larger H+-gated densities than excitatory pyramidal neurons (Ziemann et al., 2008)

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This glycolytic exhaustion, intertwined with lipid toxicity, coalesces into a self-reinforcing metabolic vortex that etches both the penumbras fate and the patients long-term functional identity, directly linking metabolic collapse to neuropsychiatric sequelae like post-stroke depression and anxiety [19, 20]