Adenosine receptors (ARs) are involved in CX
CL1-mediated short-term potentiation (STP) of
-aspartate receptor (NMDAR). (A-D) Slices pretreated for 20 minutes with AR antagonists (last 10 minutes in the graph) and then continuously treated. Inset on top: representative NMDAR component of field excitatory postsynaptic potential (NMDA-fEPSP) traces recorded in control condition, in the presence of CX3CL1 and during washout, as indicated (same time points as Figure 1). Vertical scale bar: 0.5 mV, horizontal scale bar: 20 ms. Graphs represent the average timecourse of CX3CL1 effects on NMDA-fEPSPs in the presence of AR antagonists. Points: mean ± SEM. Horizontal bar, CX3CL1 application (5 nM). (A) Slices superfusion with the non-selective AR antagonist, triazoloquinazoline (CGS15943) (25 nM) prevented CX3CL1 action (n = 9/4). (B) CX3CL1 application in the presence of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (25 nM), was effective (n = 9/5). (C) CX3CL1 application in the presence of 3-propyl-6-ethyl-5-[(ethylthio)carbonyl]-2 phenyl-4-propyl-3-pyridine carboxylate (MRS1523) (100 nM) induced a significant increase of NMDA-fEPSPs (n = 10/5). (D) 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH58261) (10 nM) prevented CX3CL1 action (n = 6/3).