ArticleNeurobiology of aging2018
Acute psychosocial stress in mid-aged male rats causes hyperthermia, cognitive decline, and increased deep sleep power, but does not alter deep sleep duration.
Article in Neurobiology of aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Establishment of a chronic insomnia rat model of sleep fragmentation using unstable platforms surrounded by water.Experimental and therapeutic medicine · 2023Article
- Cognitive Reserve in Model Systems for Mechanistic Discovery: The Importance of Longitudinal Studies.Frontiers in aging neuroscience · 2020Review
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Authors and funding
4 authors.
Funding
Abstract
Aging is associated with altered sleep architecture and worsened hippocampus-dependent cognition, highly prevalent clinical conditions that detract from quality of life for the elderly. Interestingly, exposure to psychosocial stress causes similar responses in young subjects, suggesting that age itself may act as a stressor. In prior work, we demonstrated that young animals show loss of deep sleep, deficits in cognition, and elevated body temperature after acute stress exposure, whereas aged animals are hyporesponsive on these measures. However, it is unclear if these age-altered stress responses occur in parallel over the course of aging. To address this, here we repeated the experiment in mid-aged animals. We hypothesized that mid-aged stress responses would be intermediate between those of young and aged subjects. Sixteen mid-aged (12 months) male F344 rats were implanted with EEG/EMG emitters to monitor sleep architecture and body temperature, and were trained on the Morris water maze for 3 days. On the fourth day, half of the subjects were restrained for 3 hours immediately before the water maze probe trial. Sleep architecture and body temperature were measured during the ensuing inactive period, and on the following day, endpoint measures were taken. Restrained mid-aged animals showed resistance to deep sleep loss, but demonstrated stress-induced water maze probe trial performance deficits as well as postrestraint hyperthermia. Taken in the context of prior work, these data suggest that age-related loss of sleep architecture stress sensitivity may precede both cognitive and body temperature-related stress insensitivity.
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