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Figure 1 | Molecular Brain

Figure 1

From: A role of p38 mitogen-activated protein kinase in adenosine A1 receptor-mediated synaptic depotentiation in area CA1 of the rat hippocampus

Figure 1

p38 MAPK contributes the induction of LFS-induced depotentiation. (A) Summary of experiments showing that LFS (2 Hz, 10 min) given 5 min after two trains of 100 Hz HFS almost completely reversed LTP (n = 8; ), whereas fEPSPs in slices that received HFS without LFS exhibited persistent potentiation (n = 8; ). (B) Summary of experiments showing that pretreatment of slices with the p38 MAPK inhibitor SB203580 (1 μM) blocked the induction of LFS-induced depotentiation (n = 8; ) but had no effect on the induction of LTP (n = 6; ). (C) Summary of experiments showing that pretreatment of slices with the p38 MAPK inhibitor SB239063 (1 μM) blocked the induction of LFS-induced depotentiation (n = 5; ) but had no effect on the induction of LTP (n = 4; ). (D) Summary of experiments showing that the protocol of LFS had no lasting effect on synaptic transmission in the presence of vehicle (n = 6; ) or SB203580 (n = 6; ). The superimposed fEPSP in the inset illustrates respective recordings from example experiments taken at the time indicated by number. Horizontal bars denote the period of delivery LFS or SB203580. (E) Representative immunoblots showing that the induction of LFS-induced depotentiation (DEP) is accompanied by a significant increase in p38 MAPK phosphorylation and that SB203580 (1 μM) prevented this enhancement action. Group data showing the normalization of phospho-p38 MAPK to the nonphosphorylated form was determined in each group of five experiments. In each experiment, 21–28 slices obtained from 2–3 rats were used. *, p < 0.05 (unpaired Student's t test) as compared with the control (Con) group.

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