The development of sex differences in the adrenal morphology and responsiveness in stress of rats from birth to the end of life

Senčar-Čupović, Ilinka; Milković, S.

doi:10.1016/0047-6374(76)90002-6

Cited by 46 publications

(19 citation statements)

References 14 publications

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“…Interestingly, male rats showed a greater response to the restraint stress than did females on the first and last day of stress testing. This difference between males and females in HPA response to the stressor may in part be due to sex differences in pubertal development of the HPA axis (McCormick and Mathews, 2007) as sex differences in adrenal weight emerge after 50 days of age (Sencar-Cupovic and Milkovic, 1976). Furthermore, although it appears that adolescent and adult female rats can show higher peak corticosterone responses to stress than males , females rats at both ages also show faster return to baseline (Romeo et al, 2004a,b).…”

Section: Exposure To Chronic Stress During Adolescence Induces Differmentioning

confidence: 91%

Chronic restraint stress in adolescence differentially influences hypothalamic‐pituitary‐adrenal axis function and adult hippocampal neurogenesis in male and female rats

et al. 2011

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Previous studies have shown a relationship between adversity in adolescence and health outcomes in adulthood in a sex-specific manner. Adolescence is characterized by major changes in stress-responsive regions of the brain, including the hippocampus, the site of ongoing neurogenesis throughout the lifespan. Prepubertal male and female rats exhibit different acute reactions to chronic stress compared to adults, but less is known about whether these stress-induced changes persist into adulthood. Therefore, in this study, we investigated the effects of chronic, intermittent stress during adolescence on basal corticosterone levels, dentate gyrus (DG) volume, and neurogenesis in the hippocampus of adult male and female Sprague-Dawley rats. Adolescent male and female rats were either restrained for 1 h every other day for 3 weeks from postnatal days (PDs) 30-52 at unpredictable times or left undisturbed. All rats received a single injection of bromodeoxyuridine (BrdU; 200 mg/kg) in adulthood on PD70 and were perfused 3 weeks later. Brains were processed for Ki67 (endogenous marker of cell proliferation) and BrdU (to estimate effects on cell survival). In addition, blood samples were taken during the restraint stress period and in adulthood. Results show that males and females exhibit different corticosterone responses to chronic stress during adolescence and that only adult female rats exposed to stress during adolescence show higher basal corticosterone levels compared to nonstressed controls. Furthermore, stressed females showed a reduced number of proliferating and surviving cells in the DG in adulthood compared to nonstressed same-sex controls. The majority of BrdU-labeled cells were co-labeled with NeuN, an endogenous marker of mature neurons, indicating that neurogenesis was decreased in the DG of adult female rats that had undergone chronic restraint stress in adolescence. Although male rats were more responsive to the chronic stress as adolescents showing higher corticosterone levels and reduced body weight, as adults they showed a slight increase in cell survival and no effect of adolescent stress on basal corticosterone levels. These results suggest that stress during adolescence can have effects on hypothalamic-pituitary-adrenal axis function and hippocampus plasticity in adulthood, particularly in female rats.

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Section: Exposure To Chronic Stress During Adolescence Induces Differmentioning

confidence: 91%

Chronic restraint stress in adolescence differentially influences hypothalamic‐pituitary‐adrenal axis function and adult hippocampal neurogenesis in male and female rats

et al. 2011

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“… Sencar-Cupović and Milković [433] observed no changes in plasma corticosterone levels in response to advancing age.  Landfield et al, [434] observed significant increases in aldosterone and corticosterone levels in the mid-aged (13 mo) as compared to the young (4 mo) Fisher 344 rats.…”

Section: Fisher 344 (F344) Ratsmentioning

confidence: 93%

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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“…It has now been established that basal and stress-induced adrenal steroid secretion is greater in females than in males (Critchlow et al, 1963;Kitay, 1963;Handa et al, 1994a), and that the activational effects of gonadal steroids play an integral role in this sex difference (Sencar-Cupovic and Milkovic, 1976). In females, ovariectomy reduces stressinduced CORT and ACTH, and this is reversed by estrogen treatment (Burgess and Handa, 1992;Handa et al, 1994a;Suzuki et al, 2001).…”

Section: Hypothalamic-pituitary-adrenal Axis Functionmentioning

confidence: 99%

Estrogen receptor beta in the brain: From form to function

Weiser

Foradori

Handa

2008

Brain Research Reviews

197

159

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Estrogens have numerous effects on the brain, both in adulthood and during development. These actions of estrogen are mediated by two distinct estrogen receptor (ER) systems, ER alpha (ERα) and ER beta (ERβ). In brain, ERα plays a critical role in regulating reproductive neuroendocrine function and behavior, however, a definitive role for ERβ in any neurobiological function has been slow in forthcoming. Clues to the function of ERβ in the central nervous system can be gleaned from the neuroanatomical distribution of ERβ and the phenotypes of neurons that express ERβ. ERβ immunoreactivity has been found in populations of GnRH, CRH, vasopressin, oxytocin and prolactin containing neurons in the hypothalamus. Utilizing subtype-selective estrogen receptor agonists can help determine the roles for ERβ in non-reproductive behaviors in rat models. ERβ selective agonists exert potent anxiolytic activity when animals were tested in a number of behavioral paradigms. Consistent with this, ERβ selective agonists also inhibited the ACTH and corticosterone response to stress. In contrast, ERα selective agonists were found to be anxiogenic and correspondingly increased the hormonal stress response. Taken together, our studies implicate ERβ as an important modulator of some non-reproductive neurobiological systems. The molecular and neuroanatomical targets of estrogen that are mediated by ERβ remain to be determined.A number of splice variants of ERβ mRNA have been reported in brain tissue. Imaging of eGFP labeled chimeric receptor proteins transfected into cell lines show that ERβ splice variation can alter trafficking patterns and function. The originally described ERβ (herein termed ER-β1) is characterized by possessing a high affinity for estradiol. Similar to ERα, it is localized in the nucleus and is trafficked to nuclear sites termed "hyperspeckles" following ligand binding. In contrast, ER-β2 contains an 18 amino acid insert within the ligand binding domain and as a result can be best described as a low affinity form of ERβ. A delta3 (δ3) variant of ERβ has a deletion of the 3rd exon (coding for the second half of the DNA binding domain) and as a result does not bind an estrogen response element in DNA. δ3 variants are trafficked to a unique low abundance and larger nuclear site following ligand binding. A delta4 (δ4) variant lacks exon 4 and as a result is localized to the cytoplasm. The amount of individual splice variant mRNAs varies depending upon brain region. Examination of neuropeptide promoter regulation by ERβ splice variants demonstrate that ERβ functions as a constitutively active transcription factor. Moreover, it appears that splice variation of ERβ alters its ability to regulate transcription in a promoter-dependent and ligand-dependent fashion.

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The development of sex differences in the adrenal morphology and responsiveness in stress of rats from birth to the end of life

Cited by 46 publications

References 14 publications

Chronic restraint stress in adolescence differentially influences hypothalamic‐pituitary‐adrenal axis function and adult hippocampal neurogenesis in male and female rats

Chronic restraint stress in adolescence differentially influences hypothalamic‐pituitary‐adrenal axis function and adult hippocampal neurogenesis in male and female rats

Impact of Aging on Steroid Hormone Biosynthesis and Secretion

Estrogen receptor beta in the brain: From form to function

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