Hippocampal long-term synaptic depression and memory deficits induced in early amyloidopathy are prevented by enhancing G-protein-gated inwardly rectifying potassium channel activity.

ABSTRACT: Hippocampal synaptic plasticity disruption by amyloid-β (Aβ) peptides + thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures in neuronal excitability maintenance seems to be an underlying mechanism. G-protein-gated inwardly rectifying potassium (GirK) channels control neural excitability by hyperpolarization in response to many G-protein-coupled receptors activation. Here, in early in vitro and in vivo amyloidosis mouse models, we study whether GirK channels take part of the hippocampal synaptic plasticity impairments generated by Aβ_1-42 . In vitro electrophysiological recordings from slices showed that Aβ_1-42 alters synaptic plasticity by switching high-frequency stimulation (HFS) induced long-term potentiati

SUBMITTER: Sanchez-Rodriguez I 

PROVIDER: S-EPMC7217154 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature