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This increase was concurrent with the inhibition of anti-inflammatory agents and the release of inflammatory factors
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Aos, upon binding to cell-surface receptors on neurons, disrupt signal transduction, leading to a sustained interruption of intracellular Ca 2+ signaling through increased N-methyl-D-aspartate (NMDA) receptor-dependent Ca 2+ influx [77]
10.1074/jbc.M111462200 J
