Effect of restraint stress on gonadal proopiomelanocortin peptides and the pituitary-testicular axis in rats

Mann, David R.; Orr, T. Edward

doi:10.1016/0024-3205(90)90398-b

Cited by 48 publications

(22 citation statements)

References 29 publications

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“…They also significantly interfered with hCG-induced T release, though the magnitude of the inhibitory effect of the immune challenges appeared larger than that of shocks. In contrast to what was reported by other investigators [13][14][15]61, 62], we did not observe a dissociation between LH and T levels at any time; that is, the release of both hormones was decreased by all three stressors we used. At present, the mechanisms responsible for the inhibition of Leydig cell responsiveness during acute neurogenic challenges are still disputed.…”

Section: Discussioncontrasting

confidence: 57%

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Rivier

2002

Neuroimmunomodulation

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Objective: We investigated the ability of foot shocks, endotoxemia and turpentine-induced tissue injury, to interfere with luteinizing hormone (LH) and testosterone (T) secretion, and the putative role of β-adrenergic, opiate- and corticotropin-releasing factor (CRF) receptors in these responses. Methods: Adult male rats were exposed to mild intermittent foot shocks for 1 h, administered endotoxin [lipopolysaccharide (LPS)] intravenously (i.v., 5 µg/kg), or injected with turpentine intradermally (i.m., 400 µl/kg), prior to injection with human chorionic gonadotropin (hCG, 1 U/kg i.v.). In some cases, antagonists to CRF, adrenergic or opiate receptors, or their vehicle were administered prior to the stressors. Levels of LH, T, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adrenocorticotropin (ACTH) and/or corticosterone were measured in serial blood samples. Results: All three challenges significantly lowered basal LH and T levels and blunted the T response to hCG, though the magnitude of this inhibition was significantly (p < 0.01) smaller in shocked rats (42%), compared to animals injected with LPS (92%) or turpentine (78%). Shocks, LPS and turpentine all significantly stimulated ACTH and corticosterone release, and the magnitude and time course of these responses were also stressor specific. While turpentine only increased circulating IL-6 concentrations, shocks and LPS both significantly increased circulating TNF-α and IL-6 levels, but the effect of shocks was markedly smaller. Pretreatment with propranolol did not restore T responses, while naloxone produced small and inconsistent effects. However, the CRF antagonist Astressin B, which significantly prevented stressor-induced increase in circulating levels of ACTH and corticosterone, partially reversed the inhibitory effect of LPS on hCG-induced T release. Conclusion: (1) Both neurogenic and systemic stressors lower basal plasma LH and T levels and blunt the T response to hCG. (2) LPS, whose ability to release ACTH and corticosterone was similar to that of shocks, but caused increases in circulating TNF-α and IL-6 levels that were significantly larger than those due to the other stressors, was the most potent inhibitor of the T response to hCG. (3) Neither β-adrenergic nor opiate receptors play a major role in the ability of the stressors we used to inhibit T release.

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Section: Discussioncontrasting

confidence: 57%

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Rivier

2002

Neuroimmunomodulation

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“…The inhibitory effect of chronic immobilization on plasma T has been a common finding in adult rats (5-7,10,11) attributed to reduced LH concentration (7,20). The precise mechanism of the inhibitory effect of prolonged stress on plasma T, however, is not fully understood since the changes in androgenic response are not always associated with altered LH levels (8,11,21). It was suggested that restraint stress may induce Leydig cell hyposensitivity to gonadotropin leading to a blockade of T biosynthesis at normal LH levels (21).…”

Section: Discussionmentioning

confidence: 99%

“…More recent data have shown that increased glucocorticoids may act via glucocorticoid receptors on Leydig cells, thus suppressing the testicular response to gonadotropins (11). The proopiomelanocortin (POMC)-derived peptides may also play an autocrine/paracrine role in mediating the stress-induced decline in testicular steroidogenesis (8).…”

Section: Discussionmentioning

confidence: 99%

“…Although short-or long-term immobilization is stressful to laboratory animals, the magnitude of the response depends on the intensity and duration of the stimulus (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Experiments are in progress in our laboratory using a model of aversive stimulation -6 h of daily immobilization -to investigate the effects of stress on the onset of puberty in male rats.…”

Section: Introductionmentioning

confidence: 99%

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Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

Almeida

Petenusci

Anselmo-Franci

et al. 1998

Braz J Med Biol Res

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We investigated whether chronic stress applied from prepuberty to full sexual maturity interferes with spermatogenic and androgenic testicular functions. Male Wistar rats (40 days old) were immobilized 6 h a day for 60 days. Following immobilization, plasma concentrations of corticosterone and prolactin increased 135% and 48%, respectively, while plasma luteinizing hormone and testosterone presented a significant decrease of 29% and 37%, respectively. Plasma concentration of follicle-stimulating hormone was not altered in stressed rats. Chronic stress reduced the amount of mature spermatids in the testis by 16% and the spermatozoon concentration in the cauda epididymidis by 32%. A 17% reduction in weight and a 42% decrease in DNA content were observed in the seminal vesicle of immobilized rats but not in its fructose content. The growth and secretory activity of the ventral prostate were not altered by chronic stress.

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“…However, in rats, immobilization stress reduces the plasma testosterone without affecting the plasma LH concentrations [41,42]. A study that investigated the effect of immobilization stress (immobilization of 3 hours) on testicular steroidogenesis found an 82% reduction in testosterone levels and significantly elevated levels of plasma corticosterone [43].…”

Section: Testosterone/cortisol Ratio and The Stress Systemmentioning

confidence: 99%

Use of the Testosterone/Cortisol Ratio Variable in Sports

Luccia¹

2016

TOSSJ

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Abstract:This critical review discusses the use of the testosterone/cortisol ratio in the studies of athletic performance and sports physiology. Although in most of the time physical exercise is beneficial to health, it can also be seen as a "stressor" both in men and in women. It is not completely known at what level this "physical stress" ends up its beneficial effects and begins to impair health status. In search for this putative turning point, several markers have been put forward in the last decades. One of these markers is the ratio between testosterone, considered as an anabolic hormone, and cortisol, considered as a catabolic one. Whether in search for an anabolic internal environment for strength training or to avoid performance decline during aerobic workout, the testosterone/cortisol ratio has been considered as an important physiological variable to gauge individual conditioning and responses.

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Effect of restraint stress on gonadal proopiomelanocortin peptides and the pituitary-testicular axis in rats

Cited by 48 publications

References 29 publications

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Inhibitory Effect of Neurogenic and Immune Stressors on Testosterone Secretion in Rats

Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

Use of the Testosterone/Cortisol Ratio Variable in Sports

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