ASIC channels are nonselective pores activated by mild acidification and modulating neuronal function. Expression of ASIC channels by mouse spinal cord was increased after a borderline excitotoxic stimulation. ASIC pharmacological blockers or the ASIC1a knockout phenotype intensified excitotoxicity. Electrophysiological network oscillations were suppressed by mild excitotoxic stimuli followed with ASIC block. ASIC activity was an unexpected controller of neurotoxicity to restrain spinal network damage.