Skip to main content
Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: β-Amyloid triggers aberrant over-scaling of homeostatic synaptic plasticity

Fig. 2

Recovery time course and requirement of CP-AMPARs for HSP. a1 Treatment paradigm for HSP recovery. Neurons were incubated in the appropriate treatment for 24 h, washed, then allowed to recover in fresh medium for various lengths of time. a2 Normalized mEPSC amplitudes after recovery for 24 and 96 h. Both the TTX and TTX/Aβ treatment groups returned to baseline after 96 h recovery, indicating a lack of change in the set point of neuronal activity during basal conditions (control = 12.7 ± 0.62, n = 9; TTX = 16.9 ± 0.56, n = 13; TTX 24 h recovery = 15.8 ± 0.51, n = 9; TTX 96 h recovery = 15.9 ± 1.33, n = 8; TTX/Aβ = 19.6 ± 0.54, n = 10; TTX/Aβ 24 h recovery = 17.7 ± 0.59, n = 9; TTX/Aβ 96 h recovery = 15.8 ± 1.51, n = 8). b1 Treatment paradigm of PhTx application during HSP. b2 Graph of normalized mEPSC amplitudes showing that blockade of CP-AMPARs was sufficient to occlude HSP in both the TTX and TTX/Aβ treatment groups (control = 12.5 ± 0.28, n = 7; TTX = 17.1 ± 0.52, n = 5; TTX + PhTx = 13.1 ± 0.42, n = 6; TTX/Aβ = 19.6 ± 0.79, n = 6; TTX/Aβ + PhTx = 13.5 ± 0.28, n = 6). c1 Paradigm of PhTX application after the initiation phase of HSP. Neurons were allowed to initiate HSP normally in the presence of TTX and then treated with PhTx ± Aβ. c2 Graphs show that blockade of CP-AMPARs after typical HSP initiation was sufficient to occlude Aβ-induced over-scaling of HSP (control = 12.4 ± 0.50, n = 7; TTX = 17.1 ± 0.65, n = 6; TTX → PhTx = 16.9 ± 0.68, n = 7; TTX/Aβ = 20.1 ± 0.83, n = 6; TTX/Aβ → PhTx = 17.6 ± 0.38, n = 8 cells). Mann–Whitney U test, * p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant

Back to article page
\