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Chronic restraint stress induces hippocampal memory deficits by impairing insulin signaling
- Chronic restraint stress induces hippocampal memory deficits by impairing insulin signaling
- Woo, Han Woong; Hong, Caroline Jeeyeon; Jung, Seong Hee; Choe, Seong Won; Yu, Seong-Woon
- DGIST Authors
- Yu, Seong-Woon
- Issue Date
- Molecular Brain, 11(1)
- Article Type
- Chronic restraint stress; Corticosterone; Insulin signaling; Intranasal insulin delivery; Nesting; Y-maze; NEURAL STEM-CELLS; INTRANASAL INSULIN; MINERALOCORTICOID RECEPTOR; SYNAPTIC PLASTICITY; Y-MAZE; DEATH; AUTOPHAGY; BRAIN; CORTICOSTERONE; RESISTANCE
- Chronic stress is a psychologically significant factor that impairs learning and memory in the hippocampus. Insulin signaling is important for the development and cognitive function of the hippocampus. However, the relation between chronic stress and insulin signaling at the molecular level is poorly understood. Here, we show that chronic stress impairs insulin signaling in vitro and in vivo, and thereby induces deficits in hippocampal spatial working memory and neurobehavior. Corticosterone treatment of mouse hippocampal neurons in vitro caused neurotoxicity with an increase in the markers of autophagy but not apoptosis. Corticosterone treatment impaired insulin signaling from early time points. As an in vivo model of stress, mice were subjected to chronic restraint stress. The chronic restraint stress group showed downregulated insulin signaling and suffered deficits in spatial working memory and nesting behavior. Intranasal insulin delivery restored insulin signaling and rescued hippocampal deficits. Our data suggest that psychological stress impairs insulin signaling and results in hippocampal deficits, and these effects can be prevented by intranasal insulin delivery. © 2018 The Author(s).
- BioMed Central Ltd.
- Related Researcher
Laboratory of Neuronal Cell Death
Molecular mechanisms of neuronal cell death and neurodegeneration
- Department of Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles
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