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Activity-Dependent p25 Generation Regulates Synaptic Plasticity and Aβ-Induced Cognitive Impairment

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Academic year: 2021

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Figure 1. Activity-Induced p25 Generation in Hippocampus via NMDAR and CaMKIIα (A) Primary cultured neurons were treated with NMDA (100 μM for 5 min) or glycine (200  μM for 3 min), and further incubated in conditioned media for the specified times.
Figure 2. Normal Learning but Impaired Memory Extinction in Δp35KI Mice (A) Strategy for generating the calpain-mediated, cleavage-resistant p35 protein.
Figure 3. Normal Synaptic Transmission and LTP, but Impaired LTD, in Δp35KI Hippocampus (A) The synaptic input-output relationship was obtained by plotting the slopes of evoked  fEPSPs against fiber-volley amplitude
Figure 4. p25/Cdk5 Mediates NMDA-Induced AMPAR Endocytosis by Inhibiting DARPP-32  and Activating PP1 and Calcineurin at Hippocampal Synapses
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