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In primary astrocyte cultures, glial HO-1 activation enhanced pathological iron accumulation and mitochondrial oxidative damage (Wang J

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Reduction in expression of cotransporter KCC2 is detected postinjury, triggering EIPSP (reversal potential of glycine receptor and GABA A receptor–mediated inhibitory postsynaptic potentials) depolarization resulting in spasticity below the lesion [115]