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IL-1ß, for example, has been shown to enhance the sensitivity of NMDARs by several mechanisms, including microglial recruitment and activation, and by stimulating NMDAR trafficking to the synaptic membrane.[157,269] It has also been shown that TNFα and glutamate, each in concentrations too low to initiate neurotoxicity, when combined, produce robust neurotoxicity.[79] TNF-α increased glutamate-induced neurotoxicity by a number of mechanisms, such as microglial recruitment, upregulating glutaminase, inhibition of glutamine synthetase, inhibition of EAATs and stimulation of TNFR1, which increases trafficking of GluA2-lacking AMPARs [Figure 3].[143,180] Of particular interest is the inflammation-induced enhanced trafficking of GluRs and alteration of glutamate subunits, as well as inflammatory cytokine-stimulated endocytosis of GABA receptors, which would shift the balance in the brain toward excitotoxicity

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Histological analysis Hematoxylin and Eosin (H&E) staining Paraffin-embedded skin sections were deparaffinized, rehydrated, stained with hematoxylin, differentiated in acid alcohol, neutralized in ammonia, and counterstained with eosin