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Aged rats are hypo-responsive to acute restraint: implications for psychosocial stress in aging.

Buechel HM, Popovic J, Staggs K, Anderson KL, Thibault O, Blalock EM - Front Aging Neurosci (2014)

Bottom Line: In addition, as humans age, there is a profound increase in the incidence of new onset stressors, many of which are psychosocial (e.g., loss of job, death of spouse, social isolation), and aged humans are well-understood to be more vulnerable to the negative consequences of such new-onset chronic psychosocial stress events.We then assessed hippocampus-associated behavioral, electrophysiological, and transcriptional outcomes, as well as blood glucocorticoid and sleep architecture changes.These results demonstrate that aged subjects are hypo-responsive to new-onset acute psychosocial stress, which may have negative consequences for long-term stress adaptation and suggest that age itself may act as a stressor occluding the influence of new onset stressors.

View Article: PubMed Central - PubMed

Affiliation: Blalock Laboratory, Department of Molecular and Biomedical Pharmacology, College of Medicine, University of Kentucky Lexington, KY, USA.

ABSTRACT
Cognitive processes associated with prefrontal cortex and hippocampus decline with age and are vulnerable to disruption by stress. The stress/stress hormone/allostatic load hypotheses of brain aging posit that brain aging, at least in part, is the manifestation of life-long stress exposure. In addition, as humans age, there is a profound increase in the incidence of new onset stressors, many of which are psychosocial (e.g., loss of job, death of spouse, social isolation), and aged humans are well-understood to be more vulnerable to the negative consequences of such new-onset chronic psychosocial stress events. However, the mechanistic underpinnings of this age-related shift in chronic psychosocial stress response, or the initial acute phase of that chronic response, have been less well-studied. Here, we separated young (3 month) and aged (21 month) male F344 rats into control and acute restraint (an animal model of psychosocial stress) groups (n = 9-12/group). We then assessed hippocampus-associated behavioral, electrophysiological, and transcriptional outcomes, as well as blood glucocorticoid and sleep architecture changes. Aged rats showed characteristic water maze, deep sleep, transcriptome, and synaptic sensitivity changes compared to young. Young and aged rats showed similar levels of distress during the 3 h restraint, as well as highly significant increases in blood glucocorticoid levels 21 h after restraint. However, young, but not aged, animals responded to stress exposure with water maze deficits, loss of deep sleep and hyperthermia. These results demonstrate that aged subjects are hypo-responsive to new-onset acute psychosocial stress, which may have negative consequences for long-term stress adaptation and suggest that age itself may act as a stressor occluding the influence of new onset stressors.

No MeSH data available.


Related in: MedlinePlus

Sleep architecture pre and post water maze. (A) Young vs. aged sleep stage duration before stress or water maze exposure. Total minutes in each sleep stage during the first 4 h of the active as well as rest periods are plotted (p < 0.001 for stress, aging n.s., and p < 0.05 for interaction between stress and aging in both Active and Resting periods; two way repeated measures ANOVA). (B) Influence of stress exposure on young and aged sleep architecture: (Top) Resting period immediately following stress and (Bottom) during subsequent active period (12 h later). Each sleep stage in each period was tested separately by two way ANOVA. No main effects for any stage were significant. However, the Interaction term was significant for resting period: wake (p < 0.05), REM (p < 0.05) and Deep (p < 0.01); as well as Active: Deep (p < 0.01). (For all panels *p ≤ 0.05, post hoc pairwise Fisher's LSD).
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Figure 2: Sleep architecture pre and post water maze. (A) Young vs. aged sleep stage duration before stress or water maze exposure. Total minutes in each sleep stage during the first 4 h of the active as well as rest periods are plotted (p < 0.001 for stress, aging n.s., and p < 0.05 for interaction between stress and aging in both Active and Resting periods; two way repeated measures ANOVA). (B) Influence of stress exposure on young and aged sleep architecture: (Top) Resting period immediately following stress and (Bottom) during subsequent active period (12 h later). Each sleep stage in each period was tested separately by two way ANOVA. No main effects for any stage were significant. However, the Interaction term was significant for resting period: wake (p < 0.05), REM (p < 0.05) and Deep (p < 0.01); as well as Active: Deep (p < 0.01). (For all panels *p ≤ 0.05, post hoc pairwise Fisher's LSD).

Mentions: EEG and EMG data were scored for duration of Wake, REM sleep, light sleep, and deep sleep. The first 4 h of Resting and Active periods were evaluated before spatial water maze training, and again after restraint stress. As in prior work, control aged subjects showed less active period wake and less resting period deep sleep than young (Figure 2A). Restrained young animals showed significantly more wakefulness, and less REM and deep sleep during the inactive period, while aged animals showed only elevated REM sleep (Figure 2B upper). During the post-stress active period, young rats only showed a significant elevation in deep sleep (Figure 2B lower). Note that previous work has shown, in both humans and rodents, that increased active period deep sleep is related to poor cognition (Reid et al., 2006; Buechel et al., 2011)


Aged rats are hypo-responsive to acute restraint: implications for psychosocial stress in aging.

Buechel HM, Popovic J, Staggs K, Anderson KL, Thibault O, Blalock EM - Front Aging Neurosci (2014)

Sleep architecture pre and post water maze. (A) Young vs. aged sleep stage duration before stress or water maze exposure. Total minutes in each sleep stage during the first 4 h of the active as well as rest periods are plotted (p < 0.001 for stress, aging n.s., and p < 0.05 for interaction between stress and aging in both Active and Resting periods; two way repeated measures ANOVA). (B) Influence of stress exposure on young and aged sleep architecture: (Top) Resting period immediately following stress and (Bottom) during subsequent active period (12 h later). Each sleep stage in each period was tested separately by two way ANOVA. No main effects for any stage were significant. However, the Interaction term was significant for resting period: wake (p < 0.05), REM (p < 0.05) and Deep (p < 0.01); as well as Active: Deep (p < 0.01). (For all panels *p ≤ 0.05, post hoc pairwise Fisher's LSD).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3921565&req=5

Figure 2: Sleep architecture pre and post water maze. (A) Young vs. aged sleep stage duration before stress or water maze exposure. Total minutes in each sleep stage during the first 4 h of the active as well as rest periods are plotted (p < 0.001 for stress, aging n.s., and p < 0.05 for interaction between stress and aging in both Active and Resting periods; two way repeated measures ANOVA). (B) Influence of stress exposure on young and aged sleep architecture: (Top) Resting period immediately following stress and (Bottom) during subsequent active period (12 h later). Each sleep stage in each period was tested separately by two way ANOVA. No main effects for any stage were significant. However, the Interaction term was significant for resting period: wake (p < 0.05), REM (p < 0.05) and Deep (p < 0.01); as well as Active: Deep (p < 0.01). (For all panels *p ≤ 0.05, post hoc pairwise Fisher's LSD).
Mentions: EEG and EMG data were scored for duration of Wake, REM sleep, light sleep, and deep sleep. The first 4 h of Resting and Active periods were evaluated before spatial water maze training, and again after restraint stress. As in prior work, control aged subjects showed less active period wake and less resting period deep sleep than young (Figure 2A). Restrained young animals showed significantly more wakefulness, and less REM and deep sleep during the inactive period, while aged animals showed only elevated REM sleep (Figure 2B upper). During the post-stress active period, young rats only showed a significant elevation in deep sleep (Figure 2B lower). Note that previous work has shown, in both humans and rodents, that increased active period deep sleep is related to poor cognition (Reid et al., 2006; Buechel et al., 2011)

Bottom Line: In addition, as humans age, there is a profound increase in the incidence of new onset stressors, many of which are psychosocial (e.g., loss of job, death of spouse, social isolation), and aged humans are well-understood to be more vulnerable to the negative consequences of such new-onset chronic psychosocial stress events.We then assessed hippocampus-associated behavioral, electrophysiological, and transcriptional outcomes, as well as blood glucocorticoid and sleep architecture changes.These results demonstrate that aged subjects are hypo-responsive to new-onset acute psychosocial stress, which may have negative consequences for long-term stress adaptation and suggest that age itself may act as a stressor occluding the influence of new onset stressors.

View Article: PubMed Central - PubMed

Affiliation: Blalock Laboratory, Department of Molecular and Biomedical Pharmacology, College of Medicine, University of Kentucky Lexington, KY, USA.

ABSTRACT
Cognitive processes associated with prefrontal cortex and hippocampus decline with age and are vulnerable to disruption by stress. The stress/stress hormone/allostatic load hypotheses of brain aging posit that brain aging, at least in part, is the manifestation of life-long stress exposure. In addition, as humans age, there is a profound increase in the incidence of new onset stressors, many of which are psychosocial (e.g., loss of job, death of spouse, social isolation), and aged humans are well-understood to be more vulnerable to the negative consequences of such new-onset chronic psychosocial stress events. However, the mechanistic underpinnings of this age-related shift in chronic psychosocial stress response, or the initial acute phase of that chronic response, have been less well-studied. Here, we separated young (3 month) and aged (21 month) male F344 rats into control and acute restraint (an animal model of psychosocial stress) groups (n = 9-12/group). We then assessed hippocampus-associated behavioral, electrophysiological, and transcriptional outcomes, as well as blood glucocorticoid and sleep architecture changes. Aged rats showed characteristic water maze, deep sleep, transcriptome, and synaptic sensitivity changes compared to young. Young and aged rats showed similar levels of distress during the 3 h restraint, as well as highly significant increases in blood glucocorticoid levels 21 h after restraint. However, young, but not aged, animals responded to stress exposure with water maze deficits, loss of deep sleep and hyperthermia. These results demonstrate that aged subjects are hypo-responsive to new-onset acute psychosocial stress, which may have negative consequences for long-term stress adaptation and suggest that age itself may act as a stressor occluding the influence of new onset stressors.

No MeSH data available.


Related in: MedlinePlus