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Fig. 2 | Alzheimer's Research & Therapy

Fig. 2

From: Activation of PLCβ1 enhances endocannabinoid mobilization to restore hippocampal spike-timing-dependent potentiation and contextual fear memory impaired by Alzheimer’s amyloidosis

Fig. 2

m-3M3FBS, a PLC activator, restores PLCβ-dependent S-eCB mobilization and PLCβ1 protein levels disrupted by AβO. a Time courses of the changes in mean eIPSC amplitudes following a S-eCB mobilization paradigm consisting of 60-s-long postsynaptic CA1 PC spikes (spike, at 1 Hz) with DHPG (50 μM) and LY367385 (100 μM) application in the presence of a PLCβ blocker, U73122 (5 μM) (+ U73122) in DMSO-treated (black circle, n = 9), AβO-treated (red circle, n = 10), and scrambled AβO-treated rat hippocampal slices (empty circle, n = 8). b The mean of the normalized eIPSC amplitude of the first 10 s after S-eCB mobilization protocol in rat hippocampal slice treated with DMSO (black bar), AβO (red bar), and scrambled AβO (empty bar). cd Same as a and b but for eIPSCs in the presence of a PLC activator, m-3M3FBS (30 μM) (+ m-3M3FBS) in DMSO-treated (black, n = 7), AβO-treated (magenta, n = 8), and scrambled AβO-treated rat hippocampal slices (empty, n = 8). Inset: a, c representative eIPSC traces at indicated time points (1, 2). e Representative photomicrograph of western blots of PLCβ1 (top, 150 kDa) and GAPDH (down, 35 kDa) proteins from DMSO-treated (left lane), AβO-treated (middle lane) rat hippocampal slices, and in the presence of m-3M3FBS (30 μM) in AβO-treated rat hippocampal slices (right lane). f PLCβ1 protein levels normalized to the GAPDH protein levels in DMSO-treated (black, n = 8), AβO-treated rat hippocampal slices (red, n = 8), and in the presence of m-3M3FBS AβO-treated rat hippocampal slices (magenta, n = 7). Statistical tests: b, d, f One-way ANOVA with post hoc Tukey’s test, # p < 0.05, ns: p > 0.05. Data are represented as mean ± SEM

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