Fig. 9

Effects of inflammatory cytokines on Glu synthesis, release and uptake. TNF-α and IL-1β can promote the synthesis and release of Glu, activate mGluR and AMPAR on the postsynaptic membrane, and cause mEPSC enhancement and neuronal excitotoxicity in postsynaptic neurons. Moreover, microglia-derived IL-1β can inhibit the expression of EAAT, reduce the transfer of Glu from the synaptic cleft to astrocytes, and aggravate the hyperexcited stimulation of postsynaptic neurons by Glu. In addition, astrocytes absorb less Glu, transform and generate less Gln, and transport less Gln to glutamatergic neurons, a process that would balance Glu release from glutamatergic neurons to a certain extent