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. 2004 Jul 28;24(30):6799–6809. doi: 10.1523/JNEUROSCI.5463-03.2004

Figure 7.


Figure 7.

1-42 treatment decreased BDNF-induced Akt activation. A, Phosphorylated Akt (P-Akt) levels were determined with an antibody specific to P-Akt. Exposure to BDNF (50 ng/ml) for 10 min increased the amount of P-Akt. Pretreatment with 5 or 10 μm1-42 suppressed the effect of BDNF. Aβ1-42 had no effect on total Akt (T-Akt) levels. B, Quantification of the effect of pretreatment with 5 or 10 μm1-42. Estimates are the mean ± SEM (n = 3) expressed in terms of P-Akt levels obtained in the BDNF-exposed cultures. The effect of Aβ1-42 at 10 μm was significant (*p < 0.05, unpaired Student's t test). C, Pretreatment with 10 μm1-42 decreased BDNF-induced Akt activity, measured by the phosphorylation of glycogen synthase kinase-3α/β (GSK-3α/β), a substrate of Akt, using immunoprecipitated Akt from cell lysates as described in Materials and Methods. D, Quantification of the effects of pretreatment with 10 μm1-42. Estimates are the mean ± SEM (n = 3) expressed in terms of phosphorylated GSK-3α/β levels obtained in the BDNF-exposed cultures. The effect of Aβ1-42 was significant (*p < 0.05, unpaired Student's t test).