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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

Fig. 5

Young APP/PS1–21 mice are devoid of amyloid deposit and reactive astrocyte whereas gradually overexpress TRPA1. a Thioflavin S staining for β-amyloid deposits (green) and NeuN immunostaining (magenta) in the hippocampus of 1-month-old (left) and 6-month-old (right) APP/PS1–21 mice showing the progression of the number of amyloid deposits. b GFAP (cyan) and NeuN (magenta) immunostainings in the stratum radiatum of a P30 WT (left) and APP/PS1–21 (right) mice. c Western-blot analysis of protein levels of TRPA1 channels in hippocampus extracts from P19 and P30 WT and APP/PS1–21 mice (3 different extracts of P30 WT and APP/PS1–21 mice are shown). Histogram showing quantification of TRPA1 channels expression normalized to protein loading levels (n = 6 hippocampus in each group at P19 and 8 hippocampus in each group at P30). d Western-blot analysis of protein levels of GFAP in hippocampus extracts from P19 and P30 WT and APP/PS1–21 mice (extracts of same P30 lysates depicted in c are shown). Histogram showing quantification of GFAP expression normalized to protein loading levels (n = 7 hippocampus in each group at P19 and P30). Results are compared with the WT mice with *, p < 0.05; **, p < 0.01 and ***, p < 0.001

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