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. 2003 Mar 15;23(6):2371–2382. doi: 10.1523/JNEUROSCI.23-06-02371.2003

Fig. 3.

Fig. 3.

Role of MEK in the effects of endocannabinoids in rat hippocampal slices. A, Rat hippocampal slices were incubated as described in Materials and Methods, for 50 min before the addition of vehicle (Control), 1 μmanandamide, or 1 μm 2-AG for 5 min. Homogenates (60 μg of protein per sample) were analyzed by immunoblotting with antibodies specific for the phosphorylated forms of MEK1/2. Quantification of P-MEK immunoreactivity (mean ± SEM): controls 100 ± 8, anandamide 857 ± 29, 2-AG 514 ± 57 (F(2,5) = 226, p < 0.001; t test treated vs control: p< 0.0001). B, Slices were treated with the same compounds as in A, or with 0.2 μm LPA, in the absence or in the presence of 50 μm PD98059 or 30 μm U0126, two MEK inhibitors. Homogenates were analyzed for active dually phosphorylated ERK by immunoblotting.C, Quantification of the results for P-ERK2 as described in the legend to Figure 1. Data correspond to mean ± SEM. Statistical analysis was done with ANOVA (F(11,45 = 7.4; p< 0.0001) followed by t test (treated vs control: ***p < 0.001; treated in the presence of MEK inhibitor vs in its absence: ° p < 0.05).