AI Article Synopsis
- Stress is a natural part of life that can lead to neuropsychiatric disorders, making effective stress management vital for health.
- The study found that ethyl pyruvate (EP) can protect against cognitive decline induced by stress by blocking the effects of the stress hormone corticosterone on long-term potentiation (LTP) in the brain.
- While EP did not reduce anxiety caused by stress, it improved cognitive function and increased neurogenesis in the hippocampus, likely through the regulation of Akt/GSK-3β signaling pathways.
Article Abstract
Stress is an inevitable part of life and, simultaneously, a stimulus that can trigger various neuropsychiatric disorders. Therefore, proper stress management is essential for maintaining a healthy life. In this study, we investigated the suppression of stress-induced cognitive deficit by controlling changes in synaptic plasticity caused by stress and confirmed that ethyl pyruvate (EP) has such an effect. Corticosterone, a stress hormone, suppresses long-term potentiation (LTP) in mouse acute hippocampal slices. EP blocked the LTP inhibitory effect of corticosterone by regulating GSK-3β function. Restraint stress for 2 weeks increased the anxiety levels and caused the cognitive decline in the experimental animals. Administration of EP for 14 days did not affect the increase in anxiety caused by stress but improved cognitive decline caused by stress. In addition, the decrease in neurogenesis and synaptic function deficits in the hippocampus, which cause of cognitive decline due to stress, were improved by EP administration. These effects appear via regulation of Akt/GSK-3β signaling, as in in vitro studies. These results suggest that EP prevents stress-induced cognitive decline through the modulation of Akt/GSK-3β-mediated synaptic regulation.
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| http://dx.doi.org/10.1016/j.lfs.2023.121901 | DOI Listing |
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