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. Author manuscript; available in PMC: 2019 Apr 25.
Published in final edited form as: Cell Rep. 2019 Apr 16;27(3):658–665.e4. doi: 10.1016/j.celrep.2019.03.041

Figure 3. Ab Blocks LTP-Induced CaMKII Accumulation at Excitatory Synapses.

Figure 3.

(A) Representative images of CaMKIIα in hippocampal neuron before and after treatment with Aβ peptide (500 nM; labeled with Alexa Fluor 647) and cLTP stimulation. Scale bar indicates 5 μm.

(B) Aβ application (500 nM for 45 min, unless indicated otherwise) does not affect the basal localization of endogenous CaMKIIα in hippocampal neurons, as detected with an intrabody (n = 13 neurons; unpaired Student’s t test).

(C) Preincubation with Aβ blocks subsequent cLTP-induced CaMKII movement to excitatory synapses. A control peptide with scrambled Ab sequence did not affect the cLTP-induced CaMKII movement (n = 19, 11, 11 neurons; one-way ANOVA, Tukey’s post hoc test, ***p < 0.001).

(D) Aβ does not affect the cLTD-induced CaMKII movement to inhibitory synapses (n = 15, 12 neurons; unpaired Student’s t test).

(E and F) cLTP-induced CaMKII movement to excitatory synapses is inhibited by 500 nM and 50 nM Aβ, but not 5 nM Aβ (E; n = 14, 16, 16, 17 neurons; one-way ANOVA, Tukey’s post hoc test, ***p < 0.001) and by 45-min and 20-min, but not 5-min, preincubation with Aβ (F; n = 9, 17, 21, 11 neurons; one-way ANOVA, Tukey’s post hoc test, ***p < 0.001).

(G) Ionomycin (5 μM) induces CaMKIIα movement to excitatory synapses, which is also blocked by Aβ (n = 10, 13 neurons; unpaired Student’s t test, *p < 0.05).