Skip to main content
. 2009 Jun;23(6):1969–1977. doi: 10.1096/fj.08-121152

Figure 5.

Figure 5.

The change in synaptic transmission resulting from endogenous secretion of Aβ42 can be produced by exogenous application of synthetic Aβ42 oligomers or fibrils and reversed by drug application. A) Representative Western blots of oligomeric (left) and fibrillar Aβ42 (right). Left panel: dimer, trimer, and tetramer of Aβ42 in oligomer-forming conditions; no indication of higher molecular weight aggregates and smears. Right panel: in fibril-forming conditions, large Aβ42 aggregates with higher molecular weight remain in the well. B) Application of synthetic oligomeric and fibrillar Aβ42 peptides (10 μM) for 30 min depressed and enhanced EJCs, respectively. Experiments were conducted in 0.4 and 0.2 mM Ca2+ for oligomers (n=11/treatment) and fibrils (n=8/treatment), respectively. C) Incubation with 1,2-naphthoquinone (0.15 μM) for 30 min rescued the synaptic transmission deficit in elav/y; Aβ/+ larvae. n = 6/genotype. D) Application of apegenin (15 μM) for 30 min reversed the enhancement of EJCs in G7/+; Aβ/+ larvae. n = 4/genotype. *P < 0.05; **P < 0.02. Scale bars = 10 nA (vertical); 7.5 ms (horizontal).