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. 2012 Oct 3;7:50. doi: 10.1186/1750-1326-7-50

Figure 4.

Figure 4

Functional deficits in the HCN1 channel facilitate Aβ generation. (A) Quantification of endogenous murine Aβ40 and Aβ42 in the cortex of 4-month-old HCN1+/+, HCN1+/-, and HCN1-/- mice by using the sELISA system (left panels). Statistical analysis was performed using the two-tailed Mann–Whitney U-test (average ± SEM, n = 5, **p < 0.01). (B) Quantification of Aβ40 and Aβ42 secreted into the culture medium by N2a cells by using the sELISA system. FLAG-APP or FLAG-APP and HCN1 were transiently overexpressed in the cells with (+) or without (−) 10 μM ZD7288 (left panels). Statistical analysis was performed using one-way analysis of variance followed by Tukey’s multiple comparison test (average ± SEM, n = 4, ***p < 0.001). Expression levels of APP and HCN1 was confirmed by immunoblotting (right panels in A and B).