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. Author manuscript; available in PMC: 2007 Oct 23.
Published in final edited form as: Curr Neurovasc Res. 2006 May;3(2):107–117. doi: 10.2174/156720206776875830

Fig. (1). mGluRIs significantly increase Akt1 activity during free radical exposure, but PI 3-K blockade or gene silencing eliminates Akt1 activity.

Fig. (1)

(A and B) Neuronal protein extracts (50 μg/lane) were immunoblotted with anti-phosphorylated -GSK-3α/β (p-GSK-3α/β) following incubation with the Akt1 substrate GSK-3α/β. Exposure to DHPG (750 μg/ml) or NO (NOC-9 (shown) or SNP, 300 μM) significantly increased p-GSK-3α/β expression. Application of the inhibitors of PI 3-K wortmannin (W, 500 nM) or LY294002 (LY, 10 μM) or gene silencing of Akt1 expression were sufficient to block the expression of p-GSK-3α/β in the presence of DHPG during NO. In (A) and (B), band density was performed using the public domain NIH Image program (developed at the U.S. National Institutes of Health and available at http://rsb.info.nih.gov/nih-image/) (*P<0.01 vs. control; †P<0.01 vs. DHPG/NO or DHPG). In all cases, control = untreated neurons.