Accumulation of Exogenous Amyloid-Beta Peptide in Hippocampal Mitochondria Causes Their Dysfunction: A Protective Role for Melatonin
Figure 3
Aβ in mitochondria, particularly on cristae of the inner membrane accompanied by severe disruption of the organelle. (a) Deposits of Aβ aggregates into the hippocampal adjacent cortex 36 hours after injection, as shown by DAB-revealed horseradish peroxidase immunohistochemistry (40x). Congophilic amyloid deposits remained visible up to 21 days following the intracerebral injection (data not shown). (b) Aβ immunoreactivity (white arrows) within mitochondria 36 hours following the injection of into hippocampus CA1 pyramidal neurons at 35000x magnification. The same anti-Aβ polyclonal antibody used in the regular immunohistochemistry was used in this procedure but revealed with a 6 nm gold-labeled second antibody. Swollen mitochondria with broken cristae and its remnants intermixed with fine electron-dense dusty granule is observed. Additionally, the membrane integrity is lost and some vacuoles became evident (black arrows). (c) Highly swollen mitochondria without cristae, like enlarged sacs, containing fine electrodense granules, rupture of external mitochondrial membranes (white arrow head), and vacuolization. In this case the anti-Aβ antibody was revealed with an irrelevant secondary antibody, used as control. (d) Intact mitochondrial ultrastructure of a PBS-injected control rat (37000x).
