Acute restraint stress reverses impaired LTP in the hippocampal CA1 region in mouse models of Alzheimer's disease.
Sci Rep
; 9(1): 10955, 2019 07 29.
Article
em En
| MEDLINE
| ID: mdl-31358853
ABSTRACT
Acute stress facilitates long-term potentiation (LTP) in the mouse hippocampus by modulating glucocorticoid receptors and ion channels. Here, we analysed whether this occurs in mouse models of Alzheimer's disease (AD) with impaired LTP induction. We found that a brief 30 min restraint stress protocol reversed the impaired LTP assessed with field excitatory postsynaptic potential recordings at cornu ammonis 3-1 (CA3-CA1) synapses in both Tg2576 and 5XFAD mice. This effect was accompanied by increased phosphorylation and surface expression of glutamate A1 (GluA1) -containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Moreover, enhanced LTP induction and GluA1 phosphorylation were sustained up to 4 h after the stress. Treatment with 200 nM dexamethasone produced similar effects in the hippocampi of these mice, which supports the glucocorticoid receptor-mediated mechanism in these models. Collectively, our results demonstrated an alleviation of impaired LTP and synaptic plasticity in the hippocampal CA1 region following acute stress in the AD mouse models.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Estresse Psicológico
/
Receptores de AMPA
/
Potenciação de Longa Duração
/
Região CA1 Hipocampal
/
Doença de Alzheimer
Tipo de estudo:
Guideline
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article