Coping is a strategic approach to dealing with stressful situations. Those who use proactive coping strategies tend to accept changes and act before changes are expected. In contrast, those who use reactive coping are less flexible and more likely to act in response to changes. However, little research has assessed how coping style changes with age. This study investigated age-related changes in coping strategies and stress responsiveness and the influence of age on the processing of conditioned fear memory in 2-, 12- and 23-month-old male mice. Coping strategy was measured by comparing the escape latency in an active avoidance test and by comparing responses to a shock prod. The results showed that proactivity in coping response gradually decreased with age. Stress responsiveness, measured by stress-induced concentration of corticosterone, was also highest in 2-month-old mice and decreased with age. Consolidation of fear memory was highest in 12-month-old mice and was negatively correlated with the degree of stress responsiveness and proactivity in coping. Fear extinction did not differ among age groups and was not correlated with stress responsiveness or the proactivity of coping. However, the maintenance of extinct fear memory, which was best in 2-month-old mice and worst in 12-month-old mice, was negatively correlated with stress responsiveness but not with coping style. Age-dependent changes in the expression of glucocorticoid receptor (GR) and its regulatory co-chaperones, which are accepted mechanisms for stress hormone stimulation, were measured in the hippocampus. The expression of GR was increased at 12 months compared to other age groups. There were no differences in Hsp70 and BAG1 expression by age. These results can be summarized as follows: (1) stress responsiveness and proactivity in coping decreased with age class; (2) consolidation of fear memory was negatively correlated with both stress responsiveness and proactivity; however, maintenance of extinct fear memory was negatively correlated with stress responsiveness only; and (3) consolidation and maintenance of extinct fear memory appeared to be more influenced by factors other than stress reactivity and proactivity in coping, such as the amount of hippocampal glucocorticoid expression.
1) Background: By 2050, it is estimated that 130 million people will be diagnosed with dementia, and currently approved medicines only slow the progression. So preventive intervention is important to treat dementia. Mild cognitive impairment is a condition characterized by some deterioration in cognitive function and increased risk of progressing to dementia. Therefore, the treatment of mild cognitive impairment (MCI) is a possible way to prevent dementia. Angelica gigas reduces neuroinflammation, improves circulation, and inhibits cholinesterase, which can be effective in the prevention of Alzheimer's disease and vascular dementia and the progression of mild cognitive impairment. (2) Methods: Angelica gigas (AG) extract 1 mg/kg was administered to mildly cognitive impaired mice, models based on mild traumatic brain injury and chronic mild stress. Then, spatial, working, and object recognition and fear memory were measured. (3) Result: Angelica gigas improved spatial learning, working memory, and suppressed fear memory in the mild traumatic brain injury model. It also improved spatial learning and suppressed cued fear memory in the chronic mild stress model animals. (4) Conclusions: Angelica gigas can improve cognitive symptoms in mild cognitive impairment model mice.Nutrients 2020, 12, 97 2 of 12 Animal models are needed to study MCI and develop therapeutics. An appropriate MCI model may have symptoms aggravating with age, but with only subtle memory impairment [5]. Animal models that meet these criteria include middle-aged rodents and transgenic mice that overexpress A β at an early stage before the dementia onset [4]. Spontaneously hypertensive rats (SHRs) appear to be appropriate as MCI models for vascular dementia, since hypertensive astrogliosis, cytoskeleton breakdown, hippocampal atrophy, and cholinergic deficit prematurely appear prematurely in this animal [6][7][8]. In contrast, drug-induced memory impairment models (such as those using scopolamine, NMDA blockers, and benzodiazepines) are not appropriate because they do not represent the various aspects of MCI [5].Traumatic brain injury (TBI) is one of the most common brain injuries that causes a progressive decline of memory and cognition [9]. Unlike severe TBI, moderate to minimal TBI tends to be overlooked. However, even mild TBI can cause gradual amnesia, altered executive function, concentration disorders, depression, apathy, and anxiety [8,10,11]. In particular, repetitive head injuries, such as those caused by collision sports or motor vehicle accidents, are known to cause dementia [12]. Animal models of TBI show a decrease in cognitive function that correlates to the extent of injury, the number of impacts, and progressively worsens [13][14][15]. Therefore, the TBI model is a useful MCI research tool because it is simple, progressive, reproducible, and the severity of cognitive decline is relative to the number of impacts [16].Chronic mild stress (CMS) is a behavioral model of depression that is caused by sequential exposure to variable mild str...
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