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In addition, the release of cytokines such as tumor necrosis factor (TNF), interleukin 6 (IL-6), and interleukin 1 beta (IL-1b) by reactive astrocytes aggravate excitotoxicity since, on the one hand, these molecules stimulate the release of glutamate from these cells, and on the other hand, these cytokines increase the functionality of post-synaptic neuronal glutamate receptors (e.g., by enhancing the phosphorylation and activation of subunits of the NMDA receptor, and by increasing the surface expression of AMPA receptors) (reviewed in [20,22]) (Figure 2)

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