Reproductive and pituitary-adrenal axis parameters in normal and prenatally stressed prepubertal blue foxes (Alopex lagopus)

2003 ◽  
Vol 76 (3) ◽  
pp. 413-420 ◽  
Author(s):  
L. V. Osadchuk ◽  
B. O. Braastad ◽  
A. L. Hovland ◽  
M. Bakken

AbstractMan-animal relationships are involved in the process of fox domestication. Handling being an important part of man-animal contacts, causes stress responses in farm-bred blue foxes. The purpose of this study was to determine how prenatal stress induced by handling pregnant vixens influences certain morphometric and hormonal parameters of adrenocortical and gonadal function in the prepubertal offspring. Blue fox females were subjected to daily handling sessions, each of 1 min, in the last trimester of pregnancy (term = 52 days). Plasma concentrations of ACTH, cortisol, progesterone, oestradiol and testosterone, as well as the in vitro adrenal and gonadal production of steroids were measured by radio-immunoassay in control (C, no. = 56) and prenatally stressed (PS, no. = 56) blue fox cubs of both sexes at the age of 6 to 7 months. Prenatal stress decreased plasma concentration of cortisol (C: 31·0 (s.e. 4·3) v. PS: 22·7(s.e. 1·6) ng/ml, P < 0·05) as well as progesterone (C: 1·00(s.e. 0·10) v. PS: 0·65(s.e. 0·05) ng/ml, P < 0·05) in female cubs. Prenatal stress did not cause any changes in adrenal or gonadal weights, plasma concentrations of testosterone or oestradiol, or in vitro adrenal or gonadal steroid production, in either sex. It is concluded that persistent handling of pregnant blue foxes did not affect the prepubertal development of the reproductive system but resulted in disregulation in the hypothalamic-pituitary-adrenal axis in the female offspring.

2000 ◽  
Vol 12 (4) ◽  
pp. 119 ◽  
Author(s):  
Ludmila V. Osadchuk ◽  
Bjarne O. Braastad ◽  
Ilpo Huhtaniemi ◽  
Morten Bakken

Handling is a stressor for blue foxes. The influence of preterm handling (1 min daily) of vixens was investigated in 68, 10-day-old cubs, 34 male and 34 female. Body, gonadal and pituitary weight, ano-genital distance, gonadal testosterone and oestradiol content and in vitro production, and pituitary LH content were measured in all cubs. The gonads were frozen or incubated in vitro with, or without, added hCG (2.5 IU per sample). The gonadal incubates and homogenates were analysed for testosterone and oestradiol by radioimmunoassay and the pituitary homogenates for LH by immunofluorometric assay. The results indicate that neonatal fox gonads actively produce steroids and that there are significant sex differences in basal steroid production and response of the gonads to hCG, and in pituitary LH content. Maternal stress resulted in a significant reduction of morphometric and hormonal measures of the reproductive system in neonatal blue foxes, with more drastic effects in female cubs. Gonadal weights were lower in cubs of both sexes from stressed vixens (65.7 4.3 v. 50.6 1.8 mg for the ovaries and 23.2 1.0 v. 17.7 1.0 mg for the testes, control v. stressed animals, P<0.01). The ano-genital distance in female offspring of stressed vixens was reduced (1.1 0.04 v. 0.9 0.03 cm, P<0.01). Basal ovarian oestradiol and testosterone production were decreased in cubs from prenatally stressed animals in comparison with controls (43.5 3.5 v. 32.6 3.7 pg ovary–1 h–1 and 0.40 0.16 v. 0.12 0.03 ng ovary–1 h–1, P<0.05). Prenatal stress did not affect either pituitary weights or LH content in either sex. There were no significant differences in ano-genital distance, testicular content of testosterone, or in vitro testosterone production between control and treated male cubs. In conclusion, these findings suggest that prenatal handling stress impaired the neonatal reproductive development of the female offspring, but had no marked effects on males. Sex-specific effects of prenatal handling stress on the reproductive development in foxes may be linked with the gender differences in responses of the hypothalamus–pituitary–adreno-cortical axis to stress conditions in this species.


Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2576-2583 ◽  
Author(s):  
Dóra Zelena ◽  
Ágnes Domokos ◽  
István Barna ◽  
Zsuzsa Mergl ◽  
József Haller ◽  
...  

In adulthood the hypothalamo-pituitary-adrenal axis is controlled by both CRH and arginine vasopressin (AVP). However, in neonates CRH secretion is very low, whereas AVP secretion is fully functional. This suggests that the role of AVP is more pronounced in young than in adult rats. We investigated the role of AVP by studying stress responses in 5, 10, and 20-d-old AVP-deficient Brattleboro rats. Two different stressors were applied: 24-h maternal separation and Hypnorm Grove Oxford UK injections. In heterozygous controls (that do express AVP), both stressors increased plasma ACTH and corticosterone. The ACTH stress response disappeared in AVP-deficient rats, demonstrating that during the perinatal period, the secretion of this hormone is controlled by AVP. Surprisingly, corticosterone responses remained intact in AVP-deficient rats. Similar findings were obtained after 1-, 4-, 12-, and 24-h long maternal separations. Thus, preserved corticosterone stress responses were not explained by changes in the timing of ACTH secretion. In vitro experiments suggested that the dissociation of ACTH and corticosterone stress responses can only be partly explained by higher ACTH responsiveness of the adrenal cortex in AVP-deficient rats. Together, our results show that in neonatal periods, AVP is crucial for the expression of ACTH stress responses, but neither AVP nor ACTH is necessary for the induction of corticosterone stress responses. Discrepant ACTH and corticosterone stress responses may reflect compensatory mechanisms activated by AVP deficiency, but disparate findings suggest that they rather depict a neonate-specific mechanism of hypothalamo-pituitary-adrenal-axis control.


2001 ◽  
Vol 123 (1) ◽  
pp. 100-110 ◽  
Author(s):  
L.V. Osadchuk ◽  
B.O. Braastad ◽  
A.-L. Hovland ◽  
M. Bakken

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3649-3660 ◽  
Author(s):  
Ladan Eshkevari ◽  
Susan E. Mulroney ◽  
Rupert Egan ◽  
Lixing Lao

We have recently reported that pretreatment with electroacupuncture (EA) at stomach meridian point 36 (St36) prevents the chronic cold-stress increase in the hypothalamus-pituitary-adrenal axis (HPA), an action that may be under central control. Given that treatment for stress-related symptoms usually begins after onset of the stress responses, the objectives of the present study were to determine the efficacy of EA St36 on HPA hormones when EA St36 is given after stress was initiated, if the results are long lasting, and if blocking the glucocorticoid receptor (GR) using RU-486 had the same effects as EA St36. Adult male rats were placed in 4 groups of animals, 3 of which were exposed to cold and 1 of which was a nontreatment control group. After exposure to the cold stress, 2 groups were treated with either EA St36 or sham-EA, repeated over 10 days. The increase in ACTH and corticosterone observed in stress-only rats was prevented in EA St36 animals, and the effects remained intact 4 days after withdrawal of EA but continuation of cold stress. When the GR was blocked with RU-486, the efficacy of EA St36 remained unchanged. GR blockade did significantly elevate ACTH, which is not seen with EA St36, suggesting that EA St36 does act centrally. The elevated HPA hormones in stress-only rats were associated with a significant increase in depressive and anxious behavior; this was not observed in the stressed EA St36 animals. The results indicate that EA specifically at St36 vs sham-EA is effective in treating chronic poststress exposure.


2019 ◽  
Vol 317 (2) ◽  
pp. R289-R300 ◽  
Author(s):  
Lizath M. Aguiniga ◽  
Wenbin Yang ◽  
Ryan E. Yaggie ◽  
Anthony J. Schaeffer ◽  
David J. Klumpp ◽  
...  

Corticotropin-releasing factor (CRF) regulates stress responses, and aberrant CRF signals are associated with depressive disorders. Crf expression is responsive to arachidonic acid (AA), where CRF is released from the hypothalamic paraventricular nucleus (PVN) to initiate the hypothalamic-pituitary-adrenal axis, culminating in glucocorticoid stress hormone release. Despite this biological and clinical significance, Crf regulation is unclear. Here, we report that acyloxyacyl hydrolase, encoded by Aoah, is expressed in the PVN, and Aoah regulates Crf through the aryl hydrocarbon receptor (AhR). We previously showed that AOAH-deficient mice mimicked interstitial cystitis/bladder pain syndrome, a condition frequently associated with comorbid anxiety and depression. With the use of novelty-suppressed feeding and sucrose preference assays to quantify rodent correlates of anxiety/depression, AOAH-deficient mice exhibited depressive behaviors. AOAH-deficient mice also had increased CNS AA, increased Crf expression in the PVN, and elevated serum corticosterone, consistent with dysfunction of the hypothalamic-pituitary-adrenal axis. The human Crf promoter has putative binding sites for AhR and peroxisome proliferator-activated receptor (PPARγ). PPARγ did not affect AA-dependent Crf expression in vitro, and conditional Pparγ knockout did not alter the AOAH-deficient depressive phenotype, despite previous studies implicating PPARγ as a therapeutic target for depression. In contrast, Crf induction was mediated by AhR binding sites in vitro and increased by AhR overexpression. Furthermore, conditional Ahr knockout rescued the depressive phenotype of AOAH-deficient mice. Finally, an AhR antagonist rescued the AOAH-deficient depressive phenotype. Together, our results demonstrate that Aoah is a novel genetic regulator of Crf mediated through AhR, and AhR is a therapeutic target for depression.


Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 649-659 ◽  
Author(s):  
Elodie M. Richard ◽  
Jean-Christophe Helbling ◽  
Claudine Tridon ◽  
Aline Desmedt ◽  
Amandine M. Minni ◽  
...  

Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on behaviors linked to anxiety and depression traits in animals. We show that CBG deficiency in mice results in markedly reduced total circulating corticosterone at rest and in response to stress. Interestingly, free corticosterone concentrations are normal at rest but present a reduced surge after stress in transcortin-deficient mice. No differences were detected between transcortin-deficient mice for anxiety-related traits. However, transcortin-deficient mice display increased immobility in the forced-swimming test and markedly enhanced learned helplessness after prolonged uncontrollable stress. The latter is associated with an approximately 30% decrease in circulating levels of free corticosterone as well as reduced Egr-1 mRNA expression in hippocampus in CBG-deficient mice. Additionally, transcortin-deficient mice show no sensitization to cocaine-induced locomotor responses, a well described corticosterone-dependent test. Thus, transcortin deficiency leads to insufficient glucocorticoid signaling and altered behavioral responses after stress. These findings uncover the critical role of plasma transcortin in providing an adequate endocrine and behavioral response to stress.


Endocrine ◽  
2012 ◽  
Vol 42 (3) ◽  
pp. 684-693 ◽  
Author(s):  
Elizabeth O. Johnson ◽  
Aldo E. Calogero ◽  
Mary Konstandi ◽  
Themis C. Kamilaris ◽  
Sandro La Vignera ◽  
...  

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