Fig. 6

Deletion of AQP4 decreased clearance of soluble recombinant human α-syn A53T from the brain. a Representative micrographs showing α-syn immunoreactive products in SN of WT mice and AQP4^−/− mice at 2 h after injection of soluble human recombinant α-syn into SN. There was more obvious α-syn residue within SN of AQP4^−/− mice than WT mice. Importantly, in AQP4^−/− mice, α-syn immunoreactive signals were present within cytoplasm of TH-positive neurons (arrowhead), indicating existence of neuronal uptake of exogenous α-syn. b Percentage of α-syn positive area in SN was lower in WT mice than AQP4^−/− mice (genotype, F_(1,12) = 19.126, p = 0.001; ligament, F_(1,12) = 159.366, p < 0.0001; interaction, F_(1,12) = 18.037, p = 0.001). c-e Representative blotting bands and densitometry analysis of α-syn monomer and oligomers (monomer: genotype, F_(1,12) = 7.809, p = 0.016; injection, F_(1,12) = 80.394, p < 0.0001; interaction, F_(1,12) = 10.132, p = 0.008. oligomers: genotype, F_(1,12) = 0, p = 1; injection, F_(1,12) = 93.161, p < 0.0001; interaction, F_(1,12) = 0.065, p = 0.804) at 2 h after injection of α-syn. Data represent mean ± SEM from 4 mice per group. Data in e and f are from two independent experiments