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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. (3). Activation of mGluRI results in the inhibitory phosphorylation of FOXO3a and FOXO3a integrity is maintain with DHPG or caspase 3 inhibition during NO.

Fig. (3)

(A, B, and C) Neuronal protein extracts (50 μg/lane) were immunoblotted with anti-phosphorylated-FOXO3a (p-FOXO3a, Ser253) (A, C) or anti-total FOXO3a (B) at 6 and 12 hours (h) following with 1 hour pre-treatment with DHPG (750 μM), DEVD (50 μM), LEHD (50μM), NO (NOC-9 (shown) or SNP, 300 μM) alone, or combined DHPG (750 μM) with NO. NO led to the loss of p-FOXO3a (A, C) and the loss of total FOXO3a (B) with 12 hours, but exposure to DHPG (750 μM) or DEVD (50 μM for caspase 3 inhibition maintained p-FOXO3a (A, C) and total FOXO3a (B) at 6 and 12 hours following NO. With caspase 9 inhibition (LEHD, 50 μM), minimal p-FOXO3a expression is maintained at 12 hours which may reflect downstream caspase 3 inhibition. In (A, B, and C), 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. NO 6 h). In all cases, control = untreated neurons.