Acute restraint stress reverses impaired LTP in the hippocampal CA1 region in mouse models of Alzheimer’s disease

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 protoco...

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Bibliographic Details
Published in:Scientific reports 2019-07, Vol.9 (1), p.10955-9, Article 10955
Main Authors: Wang, Ming, Ramasamy, Vijay Sankar, Samidurai, Manikandan, Jo, Jihoon
Format: Article
Language:English
Subjects:
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Alzheimer Disease - metabolism
Alzheimer's disease
Animal models
Animals
CA1 Region, Hippocampal - metabolism
CA1 Region, Hippocampal - pathology
Dexamethasone
Disease Models, Animal
Glucocorticoid receptors
Hippocampal plasticity
Hippocampus
Humanities and Social Sciences
Ion channels
Long-Term Potentiation
Male
Mice
Mice, Inbred C57BL
multidisciplinary
Neuronal Plasticity
Phosphorylation
Receptors, AMPA - metabolism
Restraint, Physical - psychology
Science
Science (multidisciplinary)
Stress, Psychological - metabolism
Synapses
Synaptic plasticity
Synaptic Transmission
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Summary: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.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-019-47452-6