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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Neurobiol Aging. 2016 Mar 4;42:41–49. doi: 10.1016/j.neurobiolaging.2016.02.028

Figure 6. Trypsin-induced neuroprotection and ERK1/2 phosphorylation are inhibited by PS1 FAD mutation M146V.

Figure 6

Mouse cortical neuronal cultures prepared from brains expressing one (A, M146V/+) or both (B, M146V/M146V) alleles of PS1 FAD mutation M146V were treated at 7 DIV with 5.25nM trypsin for 60 minutes followed by 50μM glutamate as above. Quantification of Hoechst positive nuclei shows that trypsin does not protect neurons from glutamate in either case (A, B). Results are expressed as mean ± standard error and were calculated from four independent experiments. (C) WT, M146V/+ and M146V/M146V cortical neurons from the same littermate were treated at 7 DIV with 5.25 nM trypsin for the indicated time periods. Untreated cultures were used as controls (NT). Following incubation, cells were collected and assayed on WB for the indicated proteins. A representative blot out of 4–7 independent experiments is shown. (D) Densitometric analysis of p-ERK 1/2 in the presence of trypsin at different time points expressed as percentage of phospho-ERK 1/2 (p-ERK) to total ERK 1/2 (t-ERK) ratio that was set as 100% for control (NT). Bars represent phospho-protein to total protein ratios relative to control. *p=0.05, ** p<0.005 (Tukey’s post-hoc)