Stress impairs synaptic plasticity in triple-transgenic alzheimer's disease mice: Rescue by ryanodine

Gayane Grigoryan, Gloria Biella, Diego Albani, Gianluigi Forloni, Menahem Segal

Research output: Contribution to journalArticlepeer-review


Background: A possible contributing factor to the development of cognitive deficits in Alzheimer's disease (AD) patients involves the exposure to early life stress. Objective: We explored the impact of stress on synaptic plasticity (long-term potentiation, LTP) of 6-month-old triple-transgenic mice (3×Tg-AD). Methods: 3×Tg-AD and control (NonTg) mice were exposed to three stressors at the age of 2 and 4 months. Excitatory postsynaptic potentials were recorded in the stratum radiatum of the CA1 region of hippocampal slices, in a two-pathway paradigm. Results: Slices taken from 3×Tg-AD mice exhibited significant deficits in LTP compared with NonTg slices. Early stress led to a further decrease in LTP in these mice, while it did not affect NonTg mice. LTP in 3×Tg-AD and stressed 3×Tg-AD mice was rescued by pre-exposure to 0.2 μM ryanodine. In an attempt to find a molecular correlate for the effects of stress in the 3×Tg-AD mice, we found that stressed mice have an altered ratio of Aβ42/40 both in the cortex and hippocampus. Conclusions: Stress experiences in young adults may accelerate the cognitive loss in AD mice, adding another dimension to the plethora of factors that lead to AD.

Original languageEnglish
Pages (from-to)135-138
Number of pages4
JournalNeurodegenerative Diseases
Issue number2-3
Publication statusPublished - Jan 2014


  • Alzheimer's disease
  • Hippocampal slices
  • Stress
  • Synaptic plasticity

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology


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