Figure 2
Application of p38 MAPK inhibitor prevented the induction of adenosine A 1 receptor-mediated depotentiation. (A) Summary of experiments showing that pretreatment of slices with the adenosine A1receptor antagonist DPCPX (0.1 μM) blocked the induction of LFS-induced depotentiation (n = 5; ●) but had no effect on the induction of LTP (n = 6; ○). (B) Summary of experiments showing that application of CPA (0.2 μM) for 5 min produced a depression of fEPSPs (n = 6; ○). The fEPSP fully recovered after washout of drug. (C) Summary of experiments showing that CPA (0.2 μM; 5 min) given 5 min after two trains of 100 Hz HFS almost completely reversed LTP (n = 6; ○). Note that CPA-induced depotentiation was completely blocked by DPCPX (n = 6; ●). (D) Summary of experiments showing that pretreatment of slices with SB203580 (1 μM, n = 6; ○) or SB239063 (1 μM, n = 4; ●) blocked the CPA-induced depotentiation. (E) Representative immunoblots showing that the induction of LFS-induction depotentiation (DEP) is accompanied by a significant increase in p38 MAPK phosphorylation and that DPCPX prevented this enhancement action. Group data showing the normalization of phospho-p38 MAPK to the nonphosphorylated form was determined in each group of four experiments. In each experiment, 21–28 slices obtained from 2–3 rats were used. (F) Representative immunoblots showing that the induction of CPA-induced depotentiation (CPA-DEP) is accompanied by a significant increase in p38 MAPK phosphorylation. Note that CPA-induced increase in p38 MAPK phosphorylation was significantly blocked by DPCPX or SB203580. Group data showing the normalization of phospho-p38 MAPK to the nonphosphorylated form was determined in each group of five experiments. In each experiment, 15–20 slices obtained from 2 rats were used. *, p < 0.05 (unpaired Student's t test) as compared with the control (Con) group.