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TNF-α, which is elevated with aluminum exposure [Figure 3], is a key cytokine, triggering the release of glutamate from microglia, which occurs by up-regulating glutaminase and gap junction hemichannels.[22,26,107] In addition, this cytokine impairs glutamate uptake, suppresses glutamine synthetase, increases internalization of GABA receptors, and increases GluR2-lacking AMPA receptors.[100,120] In essence, the inflammatory cytokines enhance excitotoxicity by inhibiting glutamate uptake into microglia and astrocytes, lowering GABA receptor insertion (an inhibitory transmitter), and increasing trafficking of the gluR2 lacking AMPA receptor into the synaptic membrane (stimulatory)