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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2016 Mar 11;11(2):306–315. doi: 10.1007/s11481-016-9660-2

Figure 2. Enhancement of EPSCNR2AR and EPSCNR2BR by CCL2.

Figure 2

Panels A and B illustrate the time course and amplitude (% of baseline) of the EPSCNR2AR and EPSCNR2BR recorded, in the presence of ifenprodil (Panel A, to block NR2BR, n=10) and R-CPP (Panel B, to block NR2AR, n=12), from two different neuronal cells in the CA1 region of two different slices taken from the same animal in response to constant current stimulation of Schaffer-collateral fibers (80μA, 40μS, 0.05Hz). Each data point plots the average of three consecutive EPSCs. Note that bath application of CCL2, as indicated a horizontal bar, increased the EPSCNR2AR (A) and EPSCNR2BR (B). Above each time course graph are representative individual EPSCNR2AR (A) and EPSCNR2BR (B) taken from different time points as marked by numbers 1, 2, 3, and 4, respectively. The CCL2-induced increase of EPSCNR2AR or EPSCNR2BR was almost completely blocked by a specific NA2AR antagonist R-CPP (A) or a specific NR2BR blocker ifenprodil (B). Panel C is a bar graph exhibiting the average amplitudes of EPSCNR2AR or EPSCNR2BR before (control), during (CCL2) and post (Wash) bath application of CCL2. CCL2 enhanced both EPSCNR2AR or EPSCNR2BR. All experiments were carried out in the presence of CNQX (10μM) in the perfusate and the cells were voltage clamped at −50mV. *p<0.05.