-Serine is involved in CX
CL1 action. Graphs represent the average timecourse of N-methyl-d-aspartate receptor component of field excitatory postsynaptic potentials (NMDA-fEPSPs). Points: mean ± SEM. Black horizontal bar, CX3CL1 application (5 nM). (A) Blocking of NMDAR glycine site prevented CX3CL1 effects. Slices pretreated with 5,7-dicholorokynurenic acid (DCKA) (750 nM) for 20 minutes before CX3CL1 applications (last 10 minutes in the graph) and then continuously treated. Note the absence of CX3CL1 effect (n = 8/4). (B) Enzymatic degradation of d-serine abolished CX3CL1-mediated NMDAR modulation. Slices pretreated for 1 h and then continuously superperfused with d-amino acid oxidase (DAAO) (0.1 U/ml) and catalase (300 U/ml). Cotreatment with CX3CL1 did not increase NMDA-fEPSP slopes (n = 10/4). (C) Saturation of NMDAR glycine site by d-serine prevented CX3CL1 action. Treatment with d-serine (10 μM, open bar as indicated) increased basal NMDA-fEPSPs slope and occluded CX3CL1 effect (n = 6/4).