Fig. 7
From: Lipid microdomain modification sustains neuronal viability in models of Alzheimer’s disease
Acute ADDL-induced complex formation between IR, caveolin-1 and GD1a coincides with decreased IR phosphorylation at dendrites of primary hippocampal neurons. a Immunofluorescence depicts caveolin-1 localization at dendrites. b ADDLs bind to caveolin-1 at dendrites. c – d PLA shows that ADDLs stimulate (c) caveolin-1/GD1a and (d) IR/GD1a complex formation at dendrites. Quantification shows PLA spots/inch dendrite ((c) n = 46–50 measurements; (d) n = 29–44 measurements from 6–8 independent high power fields). e A PLA using both an IR- and a phospho-tyrosine-specific antibody indicates insulin-evoked dendritic IR phosphorylation (IR/pTyr; green). ADDL exposure decreases IR phosphorylation (white bar). However, GENZ treatment increases insulin sensitivity of dendritic IR upon ADDL exposure (grey bar). Quantification shows PLA spots/inch dendrite (n = 9–13 measurements). Cells were treated with either saline or 100nM insulin for 3 min. Dendrites were visualized with phalloidin. Unpaired two-tailed student’s t-test (if p ≤ 0.05, p ≤ 0.01, or p ≤ 0.001 results are marked with (*), (**) or (***), respectively); 1 μM ADDLs, 30 min. Scale bars: 5 μM