Evidence that the Pituitary-Adrenal Axis Does Not Cross-Adapt to Stressors: Comparison to Other Physiological Variables

Armario, Antonio; Hidalgo, Juan; Giralt, Marina

doi:10.1159/000124921

Cited by 125 publications

(72 citation statements)

References 8 publications

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“…Consistent with other reports (Armario et al, 1988;Hashimoto et al, 1988;Natelson et al, 1988;De Boer et al, 1990;Hauger et al, 1990), acute stress markedly increased plasma levels of CORT in the present experiment, an effect that showed substantial habituation following repeated stressor presentation. Thus, a one-way ANOVA performed on the CORT values revealed a significant group effect [F(3,20 .…”

Section: Resultssupporting

confidence: 94%

“…For example, acute exposure to 2.5 hr restraint stress markedly activates the PA-axis, resulting in increased plasma ACTH and CORT levels, while presentation of this same stressor daily for 1 O-l 4 d results in a decrement in the magnitude of these responses (Armario et al, 1988;Hauger et al, 1990). Daily exposure to 2 hr restraint stress for l-4 weeks (Natelson et al, 1988) or 6 hr restraint stress for 4-5 weeks (Hashimoto et al, 1988) also produces habituation of these responses.…”

mentioning

confidence: 99%

“…In fact, results from a number of studies have clearly established that habituation to repeated or prolonged presentation of a single (homotypic) stressor does not generalize to other (heterotypic) stressors. For example, rats exposed to repeated restraint stress for 2-5 weeks show habituation of PA responses to the homotypic stressor, but increased ACTH and CORT responses to tail shock (Armario et al, 1988) or ether stress (Hashimoto et al, 1988). Prolonged and/or repeated exposure to isolation, crowding, or cold stress also results in habituation of PA responses to the homotypic stressor, but increased PA response to a novel stressor (Sakellaris and Vemikos-Dannellis, 1975;Vemikos et al, 1982).…”

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confidence: 99%

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Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

et al. 1994

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Acute exposure to stress leads to activation of the pituitary-adrenal axis (PA-axis) while repeated exposure to a homotypic stressor generally results in habituation of this response. Previous studies suggested that such habituation is largely due to changes in afferents of the PA-axis. To examine where within these afferents habituation occurs, we studied the effect of acute and repeated exposure to 2 hr restraint stress on expression of c-fos mRNA, as a marker of altered neuronal activity, in brain regions previously shown to influence the activity of the PA-axis. Acute restraint stress increased expression of c-fos mRNA in cortex, hippocampus, hypothalamus, septum, and brainstem. In contrast, the effect of restraint stress on c-fos expression in the aforementioned brain regions was much smaller in animals restrained once daily for 4 d, and nonexistent in animals restrained once daily for 9 d. A similar pattern of induction and habituation of jun-B, but not zif-268, c-jun, or jun-D mRNA expression, was observed in the cortex of animals exposed to acute versus repeated restraint stress. The habituation of c-fos responses was stressor specific: exposure of restraint-adapted animals to a novel (20 min swim) stress produced an increase in levels of c-fos mRNA in every examined brain region comparable to that seen in animals exposed to this stressor for the first time. Adrenalectomy did not alter the pattern of c-fos expression induced by acute and repeated restraint stress. Therefore, activation and habituation of these c-fos responses are independent of changes in circulating levels of corticosterone.

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Section: Resultssupporting

confidence: 94%

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confidence: 99%

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confidence: 99%

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Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

et al. 1994

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“…Corticosterone levels were not significantly reduced until day 5, suggesting that reduced corticosterone secretion was, at least partially, due to reduced ACTH release. Although ACTH levels just after stress might eventually decrease with additional exposure to the stressor [31, 32], for a review], corticosterone levels are more resistant to decreasing due to chronic stress inducing enhancement of the adrenocortical responsiveness to ACTH [31]. Accordingly, in the present study, the ratio of plasma corticosterone/plasma ACTH after just 20 min IMO progressively increased over the days.…”

Section: Discussionmentioning

confidence: 60%

Recovery of the Hypothalamic-Pituitary-Adrenal Response to Stress

et al. 2000

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Pathological consequences of stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis may be related to the duration rather than to the intensity of HPA axis activation after exposure to the stressor. Consequently a fine analysis of post-stress events is of importance. The present experiments were designed to study the importance of three key factors in HPA recovery: intensity of the stressor (experiment 1), duration of exposure to the stressor (experiment 2) and previous experience of the animals with the situation (experiments 3 and 4). In experiment 1, analysis of both the response to the stressor and the poststress period showed that the stronger the stressor, the greater the area under the curve of HPA activation. In experiment 2, different groups of rats were exposed to different periods of immobilization (IMO) (20 min, 1 h and 2 h) and sampled before, during and after exposure to IMO. The speed of recovery of plasma corticotropin (ACTH) levels was not related to the duration of exposure to the stressor. In experiments 3 and 4, the influence of previous experience with the stressor was studied in rats daily exposed to 20 min IMO or daily injected with hypertonic saline (HS) for 8 days and sampled on days 1, 2, 5 and 8. Whereas a significant decline in plasma ACTH levels was not observed immediately after IMO until day 8, a single previous exposure to IMO was enough to enhance recovery 90 min after the end of exposure to IMO. Corticosterone levels were related to the number of previous experiences with the stressor only in the post-IMO period. In response to a novel stressor (forced swimming), chronic IMO rats showed a slightly impaired recovery as compared to stress-naive rats, suggesting that enhanced recovery of the HPA axis was specific for the homotypic stressor. After daily HS injections, a pattern similar to that after IMO was observed, the delayed, but not the early response of the HPA axis being reduced as a function of the number of previous experiences with the situation. Taken together, the present results suggest that the speed of recovery of the HPA axis after its activation by stressors is sensitive to the intensity of the stressors but not to their duration, and that adaptation to a repeated stressor is more apparent during the delayed HPA response.

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“…Basal CORT secretion is usually elevated and the response to the same stress which was administered repeatedly is attenuated [20]. However, when a novel stress is administered following a chronic stress, a normal, or even facilitated, HPA response is exhibited [21, 22]. Long-term stress may result in higher CORT levels after the cessation of stress, i.e.…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine-Related Effects of Long-Term, ‘Binge’ Cocaine Administration: Diminished Individual Differences in Stress-Induced Corticosterone Response

Sarnyai¹,

Dhabhar²,

McEwen³

et al. 1998

Neuroendocrinology

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Acute cocaine administration activates behavioral and neuroendocrine processes associated with the stress response. However, much less is known about the effects of chronic, long-term cocaine administration on neuroendocrine adaptations and individual vulnerability to stress. We hypothesized that chronic ‘binge’ cocaine administration may serve as a chronic pharmacological stressor leading to a hyperactivity of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis and alterations in its feedback mechanisms. In order to test this hypothesis, the effects of long-term (3 and 6 weeks) ‘binge’ pattern cocaine administration (3×15 mg/kg cocaine, i.p., daily, during the early phase of the light cycle) on body weight, adrenal gland weight, basal and stress-induced activity of the corticosterone (CORT) and basal plasma testosterone (T) levels were measured. Both 3 and 6 weeks ‘binge’ cocaine administration decreased body weight gain, increased the weight of adrenal glands and increased basal CORT levels. Plasma T levels were suppressed by both 3 and 6 weeks of cocaine treatment. No correlation was found between elevated CORT and low T levels at any time point. Neither chronic saline nor cocaine administration altered stress-induced CORT secretion. CORT levels 60 min following the restraint stress (recovery) were significantly lower than pre-stress basal levels after 3 and 6 weeks of cocaine, but not saline, administration. Moreover, initial individual differences in stress-induced CORT response, i.e. low and high responsivity to restraint prior to any saline or cocaine injections, were maintained in control rats but became diminished in cocaine-treated rats. These results indicate that chronic binge cocaine administration leads to sustained activation of the HPA axis and alters processes underlying individual vulnerability to stress.

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Evidence that the Pituitary-Adrenal Axis Does Not Cross-Adapt to Stressors: Comparison to Other Physiological Variables

Cited by 125 publications

References 8 publications

Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

Recovery of the Hypothalamic-Pituitary-Adrenal Response to Stress

Neuroendocrine-Related Effects of Long-Term, ‘Binge’ Cocaine Administration: Diminished Individual Differences in Stress-Induced Corticosterone Response

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