Chronic and Acute Dexamethasone Suppression of Stress Activation of the Adrenal Cortex in Young and Aged Rats

Riegle, Gail D.; Hess, G

doi:10.1159/000122048

Cited by 76 publications

(24 citation statements)

References 9 publications

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“…The differences in adrenocortical responsiveness to stress between young and aged groups are in agreement with our previous studies, which showed decreased control system responsiveness in aged rats to corticosteroid feedback following glucocorticoid [Riegle and H ess, 1972] or ACTH injection [Hess et al, 1970]. The increased inhibition of ether vapor stress responsiveness in young male and female groups, together with the decreased responsiveness to restraint stress in young females compared to the aged groups, suggests that the adreno cortical control mechanism in the young groups was more sensitive to the inhibitory input.…”

Section: Discussionsupporting

confidence: 93%

“…Resting plasma cortico sterone levels were measured in blood samples taken 30 to 60 sec after initial animal disturbance [Riegle and H ess, 1972]. Resting values were measured before starting the chronic restraint regime and on the day following completion of the treatment.…”

Section: Methodsmentioning

confidence: 99%

“…Experiments recently conducted in our laboratory have demonstrat ed decreased adrenocortical control system responsiveness to cortico steroid feedback in the ageing rat [Hess et a!., 1970;Riegle and H ess, 1972]. These experiments did not consider the effects of corticosteroid feedback while rats are receiving simultaneous stimulatory input as normally occurs in the stress reaction.…”

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confidence: 99%

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Chronic Stress Effects on Adrenocortical Responsiveness in Young and Aged Rats

Riegle¹

1973

Neuroendocrinology

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133

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The effect of chronic stress on adrenocorticalfunction was tested in young and aged male and female rats. The rats were subjected twice a day to 2 h restraint stress for 20 days. Adrenocortical responsiveness to stressors was decreased during the treatment in all groups. Responsiveness to ACTH injection was greater than stress responsiveness in all groups. The decrease in stress responsiveness was greater in the young than in the aged groups. The data suggest that elevated corticosterone concentrations from chronic stress adrenocortical activation result in incomplete feedback inhibition of the adrenocortical control mechanism. The increased inhibition in the young groups supports the concept of decreased adrenocortical control system sensitivity in the aged animal.

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Chronic Stress Effects on Adrenocortical Responsiveness in Young and Aged Rats

Riegle¹

1973

Neuroendocrinology

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133

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“…However, both old female and male rats secreted significantly less corticosterone in response to either ACTH treatment or ether stress compared to respective young (control) animals.  The work of Riegle and Hess [456] and Riegel [457] suggest that the ability of aged (22-32-mo) male and female rats (Long-Evans) to a negative feedback inhibition of the hypothalamic-pituitary axis is significantly impaired as compared to young (4-6-mo) adult animals.  Meaney et al, [458,459] reported elevated corticosterone levels in 16-and 24-mo old male Long-Evans rats as compared to young (3-mo) and adult (8-mo) rats.…”

Section: Long-evans (Le) Ratsmentioning

confidence: 99%

Impact of Aging on Steroid Hormone Biosynthesis and Secretion

Zaidi¹

2013

TOLSJ

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Steroid hormones are lipophilic, low-molecular weight organic compounds all of which are derived from cholesterol. They are primarily synthesized by steroidogenic glands such as gonads (ovary and testis), the adrenal gland and, during pregnancy, by the placental trophoblasts. Limited steroid synthesis also takes place in the brain. Steroid hormones are crucial for the proper functioning of the body. They mediate a wide variety of vital physiological functions, ranging from maintaining normal reproductive function and secondary sexual characteristics, to regulating virtually every metabolic process in the body. Like many age-related endocrine disorders, aging also progressively impacts the tissue-specific synthesis and secretion of steroid hormones. The goal of this review is to summarize the effects of aging on steroid hormone synthesis and secretion by the adrenal gland and gonads of both human and experimental animal models, to describe the potential involvement of excessive oxidative stress in mediating age-related alterations in steroidogenesis, and to discuss the possible underlying mechanisms involved.

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“…The aged male rat is relatively insensitive to the suppressive effects of exogenous glucocorticoids on the HPA axis (14). Furthermore, such subjects hypersecrete corticosterone, the principal glucocorticoid in the rat; specifically, aged male rats show a delay in terminating corticosterone secretion at the end of stress (15).…”

mentioning

confidence: 99%

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

Sapolsky¹,

Krey²,

McEwen³

1984

Proc. Natl. Acad. Sci. U.S.A.

620

333

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The hippocampus is the principal target site in the brain for adrenocortical steroids, as it has the highest concentration of receptor sites for glucocorticoids. The aged rat has a specific deficit in hippocampal glucocorticoid receptors, owing in large part to a loss of corticoid-sensitive neurons. This deficit may be the cause for the failure of aged rats to terminate corticosterone secretion at the end of stress, because extensive lesion and electrical stimulation studies have shown that the hippocampus exerts an inhibitory influence over adrenocortical activity and participates in glucocorticoid feedback. We have studied whether it is the loss of hippocampal neurons or of hippocampal glucocorticoid receptors in the aged rat that contributes most to this syndrome of corticosterone hypersecretion. To do this, we used two model systems for producing reversible glucocorticoid receptor depletion in the hippocampus, and we found that depletion of receptors without inducing cell loss results in corticosterone hypersecretion. Furthermore, correction of the receptor deficit results in normalization of corticosterone secretion. These results focus attention on the hippocampus as an important glucocorticoid sensor in relation to the stress response. They also provide important new physiological correlates for the remarkable plasticity of the hippocampal glucocorticoid receptor system, which is under independent control by corticosterone and by vasopressin.In the mammalian brain, the hippocampus contains the highest concentration of glucocorticoid receptors and retains the highest concentration of [3H]corticosterone after in vivo injection (1). This phenomenon was initially reported in 1968 (2), and considerable speculation still remains regarding the physiological and behavioral significance of the hippocampal uptake system (1, 3). However, the hippocampus has been persistently implicated as an inhibitory influence on the hypothalamic-pituitary-adrenocortical (HPA) axis. Destruction of the hippocampus, for example, leads to hypersecretion of glucocorticoids under basal and stressed conditions (4-9). Furthermore, stimulation of most parts of the structure inhibits stress-induced HPA activation (10-13). At least some of this inhibitory influence of the hippocampus represents mediation of feedback inhibition by glucocorticoids. For example, hippocampectomized subjects are less sensitive to the suppressive effects of exogenous glucocorticoids on HPA secretion (6). Moreover, corticotropin (ACTH) is increased after hippocampectomy and the difference in corticotropin levels between lesioned and sham-lesioned animals is abolished by adrenalectomy, suggesting that the relative increase in corticotropin due to the lesion resulted from lesion-induced disinhibition from corticoid-feedback suppression (5). This evidence that circulating glucocorticoids exert some of their feedback effects via the hippocampus suggests that such actions are mediated by the hippocampal glucocorticoid receptor. Thus, one can postulate that decr...

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Chronic and Acute Dexamethasone Suppression of Stress Activation of the Adrenal Cortex in Young and Aged Rats

Cited by 76 publications

References 9 publications

Chronic Stress Effects on Adrenocortical Responsiveness in Young and Aged Rats

Chronic Stress Effects on Adrenocortical Responsiveness in Young and Aged Rats

Impact of Aging on Steroid Hormone Biosynthesis and Secretion

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

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