Fig. 8
From: Estrogen-immuno-neuromodulation disorders in menopausal depression
Effects of inflammatory cytokines on GABA synthesis (A) and release (B, C). (A) GABA is primarily synthesized by Glu, and GAD is the main rate-limiting enzyme for GABA synthesis. The binding of IL-33 to IL-1R first activates MAPK and further activates the NF-κB signaling pathway to inhibit BDNF synthesis, leading to a decrease in GAD expression and GABA synthesis. (B, C) IL-1β can regulate different GABAergic neurons, resulting in decreased or increased GABA release and corresponding decreases or increases in the number of IPSCs. TNF-α/IL-1β/IL-6 can also decrease the expression of postsynaptic GABAAR and attenuate GABA-induced IPSC. However, IL-10 promotes GABA release from GABAergic neurons and enhances IPSC through the MAPK/PI3K signaling pathway