Skip to main content
. Author manuscript; available in PMC: 2010 Jul 27.
Published in final edited form as: Biol Psychiatry. 2009 May 15;66(8):758–768. doi: 10.1016/j.biopsych.2009.03.014

Figure 3.

Figure 3

Striatal organotypic slices from Ras-GRF1 KO mice show a marked decrease of p-ERK2 induction in response to glutamate (GLU), SKF 38393, and forskolin (Forsk) but not to brain-derived growth factor (BDNF). (A,B) Organotypic striatal slices (P4) from WT (+/+) and Ras-GRF1 KO (−/−) mice after 3 days in vitro were stimulated for 15 min either with 50 μmol/L GLU, 50 μmol/L SKF, or both (C,D) with 10 μmol/L Forsk and (E,F) with 100 ng/mL BDNF. The histograms show the mean ± SEM of p-ERK2 induction expressed as the ratio normalized to nonstimulated slices (control [CTR]). (B) Absence of Ras-GRF1 caused loss of p-ERK1/2 in response to GLU, SKF, or both (two-way analysis of variance [ANOVA], Scheffé test post hoc comparison GLU, SKF, and GLU+ SKF, *p < .01 genotype effect). (D) Forskolin-mediated activation of ERK2 is partially reduced in Ras-GRF1 slices (two-way ANOVA, Scheffé test post hoc comparison, *p < .01 genotype effect). (F) p-ERK2 is normally induced in Ras-GRF1 KO striatal slices upon BDNF in comparison with WT slices. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; other abbreviations as in Figure 1.