Figure 5.

Time course of mGluR-dependent phosphorylation of ERK1/2 in the presence and absence of TTX and iGlu inhibitors. A, Time course of ERK1/2 phosphorylation in response to DHPG applied in normal solution (a, representative Western blots; c, filled circles, summary data) or in the presence of TTX, CNQX, and CPP (b, blockers, representative Western blots; c, open circles, summary data). In ACSF, DHPG induced a significant increase of ERK1/2 phosphorylation that peaked at 5 min (241 ± 42%; n = 4; p < 0.01). In the presence of the blockers, DHPG still induced a peak increase of ERK1/2 phosphorylation at 5 min (167 ± 12%; n = 8; p < 0.01), although to a significantly less extent than in ACSF (p < 0.05). B, Effects of genistein pretreatment (30 μm; 45 min) on DHPG-induced ERK1/2 phosphorylation in ACSF (a, Western blots; c, filled circles, summary data) and in the presence of the blockers (b, Western blots; c, open circles, summary data). The peak increase in ERK1/2 phosphorylation by DHPG at 5 min was still observed in ACSF (200 ± 33%; n = 4; p < 0.05), but it was completely prevented in the presence of the blockers (92 ± 21%; n = 5; p = 0.31). C, In chelerythrine-pretreated slices (10 μm; 45 min), DHPG induced similar increases of ERK1/2 phosphorylation at 5 min in ACSF (a, Western blots; c, filled circles, summary data; at 5 min: 146 ± 13%; n = 4; p < 0.01) and in the presence of TTX, CNQX, and CPP (b, Western blots; c, open circles, summary data; at 5 min, 152 ± 6%; n = 4; p < 0.01). In ACSF, the increase at 5 min (146 ± 13%) was reduced compared with that observed in control slices (241 ± 42%; p < 0.05), whereas in the blockers the increase at 5 min (152 ± 6%) was similar to that observed in control slices (167 ± 12%; p = 0.43).