Effects on immune responses by chronic stress are modulated by aging

Odio, Mauricio; Brodish, A.; Ricardo, Manuel J.

doi:10.1016/0889-1591(87)90023-7

Cited by 25 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As reported earlier [6,21], with this procedure we observe no evi dence of age-dependent differences either with respect to electric shock detection or to the ability of the rats to perform the simple behavioral task required by this model. These are relevant considerations for a study of this type, since age-related differences have been reported with respect to threshold for electric shock detection at current levels below 0.4 mA (22,23], as well as with respect to learning more complex tasks [24,251.…”

Section: Chronic Stressorsupporting

confidence: 49%

“…These experiments were designed to determine whether prior expo sure to the long-term chronic stress regimen used in our previous stu dies [6,7] would alter age-related effects on the time-course pattern of ACTH and CORT responses elicited by a novel acute stressor. For this purpose, one group o f 8 6-month-old rats and one group of 8 20-month-old rats were exposed to a total o f 120 sessions of the shockescape procedure (4h/session; I session/day; 5 days/week) over a 6-month period.…”

Section: Experimental Designmentioning

confidence: 99%

“…For the present experiments, we exposed rats to the same chronic stress schedule that was used in our previous work [6,7] and subsequently examined ACTH and CORT responses to an acute novel stressor in 12-and 26-month-old control and chronically stressed rats. Our results support the hypothesis that chronic stress can significantly influence age-related changes in pituitary-adrenocortical function.…”

mentioning

confidence: 99%

“…To study the effects of prolonged stress exposure on several physiological markers of aging, we have utilized a system in which F-344 rats were exposed to chronic stress for 6 months (approximately 20% of the life span of this rat strain). Using this chronic stress model system, age changes were reported in the immune system [6] and in the nervous system [7], Since pituitary and adrenal hormones might be mediators of the immune and neural chan ges produced by chronic stress, we employed the same chronic stress model system for the same duration to investigate stressage interactions of the pituitary-adrenal system. Received: July I, 1988 Accepted after revision: September 8, 1988 Reports in the literature indicate that old rats are not impa ired in their ability to elicit an adrenocortical response to acute stress [8 -1 1 ] but are less able to terminate this response via glu cocorticoid-mediated feedback inhibition of ACTH release [11][12][13].…”

mentioning

confidence: 99%

See 3 more Smart Citations

Age-Dependent Effects of Chronic Stress on ACTH and Corticosterone Responses to an Acute Novel Stress

Brodish

Odio²

1989

Neuroendocrinology

View full text Add to dashboard Cite

Aging effects on the hypothalamic-pituitary-adrenocortical system have been studied primarily in the sedentary, environmentally deprived laboratory rat. Since it is known that chronic activation changes the responsiveness of the hypothalamic-pituitary-adrenocortical system, the present experiments were undertaken to determine whether age-related effects on this system would differ between sedentary and chronically stressed rats. Groups of 6- and 20-month-old F-344 rats were exposed to daily sessions of a 2-way shock-escape procedure over a 6-month period. When the rats were 12 (adult) and 26 months of age (old), pituitary-adrenocortical responses to an acute, novel stimulus were examined in young and old chronically stressed and age-matched control rats. Young and old control rats showed essentially the same corticosterone response to an acute motion stress. Chronic stress exposure increased the corticosterone response to the novel acute stressor in young but not in old rats. ACTH levels in response to acute stress were significantly reduced in old control rats compared to young control animals. Chronic stress did not change the ACTH acute stress response in young animals, whereas in old animals chronic stress elevated the ACTH responsiveness so that the old rats showed stress-induced ACTH levels that were comparable to the young animals. In conclusion, the effects of chronic stress on the function of the hypothalamic-pituitary-adrenocortical system are age-dependent, and environmental factors can significantly influence the progression of aging of the hypothalamic-pituitary-adrenal system.

show abstract

Section: Chronic Stressorsupporting

confidence: 49%

Section: Experimental Designmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Age-Dependent Effects of Chronic Stress on ACTH and Corticosterone Responses to an Acute Novel Stress

Brodish

Odio²

1989

Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…A proper understanding of how the immune system initially responds to and then either adapts or fails to adapt to the particular stressor, if it is allowed to persist, needs to investigate func tion at various intervals following the initiation of stressor exposure. Observations that laboratory animals do not show profound alterations in immune activity following long term stressor exposure (weeks to months) [ 108] indicate that lymphoid cells have the capacity to adapt to new conditions in their microenvironment. The presence o f such adaptation clearly serves to maintain homeostasis and the ability o f the immune system to fulfill its role of host defense.…”

Section: Duration Intensity Anti Frequency Of Stressor Exposurementioning

confidence: 99%

Stressor-lnduced Alterations of Immune Function: Mechanisms and Issues

Kusnecov

Rabin²

1994

Int Arch Allergy Immunol

View full text Add to dashboard Cite

This paper reviews the role of catecholamines and the hypothalamic-pituitary-adrenal system in the mediation of stress-induced immune changes in both human and animal subjects. There is evidence to support the importance of these factors in mediating stressor effects on certain immune parameters, but further research is needed to define the specific circumstances in which they are relevant. Therefore, discussion of such issues as sex, genotype, stress history, environment, and stressor characteristics is provided to suggest possible ways to increase our understanding of stressor effects on immune function. Since the imposition of a stressor disrupts physiological homeostasis, understanding the capacity of the immune system to function under such conditions is of prime importance in predicting disease onset and outcome.

show abstract

A unifying hypothesis of Alzheimer's disease. III. Risk factors

Heininger

2000

Hum. Psychopharmacol. Clin. Exp.

View full text Add to dashboard Cite

Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.

show abstract

Effects on immune responses by chronic stress are modulated by aging

Cited by 25 publications

References 25 publications

Age-Dependent Effects of Chronic Stress on ACTH and Corticosterone Responses to an Acute Novel Stress

Age-Dependent Effects of Chronic Stress on ACTH and Corticosterone Responses to an Acute Novel Stress

Stressor-lnduced Alterations of Immune Function: Mechanisms and Issues

A unifying hypothesis of Alzheimer's disease. III. Risk factors

Contact Info

Product

Resources

About