Reversal of the hypothalamo-pituitary–adrenal response to oestrogens around puberty

Evuarherhe, Obaro; Leggett, James D.; Waite, Eleanor; Kershaw, Yvonne M.; Lightman, Stafford L.

doi:10.1677/joe-09-0175

Cited by 27 publications

(21 citation statements)

References 37 publications

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“…Previous studies have used either implants filled with nothing (glue, Kudwa et al, 2009; Heideman et al, 2010; Wood and Rice 2013;) or implants filled with the vehicle base (cholesterol, Evuarherhe et al, 2009; Bohacek and Daniel, 2010; Wang et al, 2011), but not both. Given our recent finding that there may be differences in these two types of “control” conditions (McLaughlin et al, 2010), we implemented both types of implants.…”

Section: Methodsmentioning

confidence: 99%

Cholesterol and perhaps estradiol protect against corticosterone-induced hippocampal CA3 dendritic retraction in gonadectomized female and male rats

et al. 2013

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Chronic stress or glucocorticoid exposure simplifies hippocampal CA3 apical dendritic arbors in male rats. In contrast to males, chronic stress either reduces CA3 basal branching or exerts no observable morphological effects in gonadally intact female rats. Under conditions that females display stress-induced CA3 dendritic retraction, such as following ovariectomy, chronic exposure to 17β-estradiol or cholesterol can negate these changes. Whether glucocorticoids produce CA3 dendritic retraction in ovariectomized females and whether neuroprotection from 17β-estradiol or cholesterol is sex-specific remains unknown. The current study examined the effects of chronic glucocorticoid exposure, in conjunction with 17β-estradiol or cholesterol administration, on hippocampal CA3 dendritic complexity. Adult male and female Sprague-Dawley rats were gonadectomized and implanted with 25% 17β-estradiol in cholesterol, 100% cholesterol, or blank Silastic capsules. Rats were then assigned to either a 21-day corticosterone (CORT) drink (400µg/mL CORT, 2.4% ethanol in tap water) or tap water (Tap, 2.4% ethanol in tap water) treatment. Brains were processed for Golgi staining, and hippocampal CA3 dendritic architecture was quantified. Results showed 21-day CORT administration reduced hippocampal CA3 apical dendritic branch points, CA3 apical dendritic length, body weight gain, and adrenal weights compared to male and female control counterparts. Furthermore, male and female rats implanted with Silastic capsules containing cholesterol or 25% 17β-estradiol in cholesterol were protected from CORT-induced CA3 apical dendritic branch reduction. No effects were observed in the CA3 basal dendritic arbors. The present results demonstrate that CORT produces hippocampal CA3 dendritic retraction in gonadectomized male and female rats and that cholesterol and 25% 17β-estradiol in cholesterol prevent this dendritic simplification.

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Section: Methodsmentioning

confidence: 99%

Cholesterol and perhaps estradiol protect against corticosterone-induced hippocampal CA3 dendritic retraction in gonadectomized female and male rats

et al. 2013

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“…However, activational effects of androgen to suppress corticosterone secretion contribute to regulation in adulthood (McCormick & Mathews, 2007; McCormick, Mathews, Thomas, & Waters, 2010). In female rats, the onset of estrous cyclicity and estradiol secretion allow them to maintain high, adolescent- like stress responses through activational effects at multiple sites including CRF production, glucocorticoid feedback and others (Evuarherhe, Leggett, Waite, Kershaw, & Lightman, 2009; Veldhuis et al, 2013). …”

Section: Sexual Differentiation Of the Brain: The Role Of Genes Amentioning

confidence: 99%

Emergence of sex differences in the development of substance use and abuse during adolescence

Kuhn

2015

Pharmacology & Therapeutics

147

109

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Substance use and abuse begins during adolescence. Male and female adolescent humans initiate use at comparable rates, but males increase use faster. In adulthood, more men than women use and abuse addictive drugs. However, some women progress more rapidly from initiation of use to entry into treatment. In animal models, adolescent males and females consume addictive drugs similarly. However, reproductively mature females acquire self-administration faster, and in some models, escalate use more. Sex/gender differences exist in neurobiologic factors mediating both reinforcement (dopamine, opioids) and aversiveness (CRF, dynorphin), as well as intrinsic factors (personality, psychiatric co-morbidities) and extrinsic factors (history of abuse, environment especially peers and family) which influence the progression from initial use to abuse., Many of these important differences emerge during adolescence, and are moderated by sexual differentiation of the brain. Estradiol effects which enhance both dopaminergic and CRF-mediated processes contribute to the female vulnerability to substance use and abuse. Testosterone enhances impulsivity and sensation seeking in both males and females. Several protective factors in females also influence initiation and progression of substance use including hormonal changes of pregnancy as well as greater capacity for self-regulation and lower peak levels of impulsivity/sensation seeking. Same sex peers represent a risk factor more for males than females during adolescence, while romantic partners increase risk for women during this developmental epoch. In summary, biologic factors, psychiatric co-morbidities as well as personality and environment present sex/gender-specific risks as adolescents begin to initiate substance use.

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“…ACTH then acts on the adrenal cortex to release glucocorticoids, cortisol in humans and corticosterone (CORT) in rodents, into the systemic circulation setting up a negative feedback loop by which CORT acts on the hypothalamus and pituitary gland to decrease further release of CRH, AVP, and ACTH. During pubertal development, the brain and HPA axis undergo extensive maturational processing, characterized by altered HPA axis reactivity, increased synaptic connections, and differential responsiveness to the effects of gonadal steroid hormones [5], [6], [7], [8], [9]. These studies indicate that the successful shaping of mature HPA function that occurs during pubertal development may be extremely vulnerable to the detrimental effects of alcohol.…”

Section: Introductionmentioning

confidence: 98%

Binge-Pattern Alcohol Exposure during Puberty Induces Long-Term Changes in HPA Axis Reactivity

et al. 2011

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Adolescence is a dynamic and important period of brain development however, little is known about the long-term neurobiological consequences of alcohol consumption during puberty. Our previous studies showed that binge-pattern ethanol (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis, as manifested by alterations in corticotrophin-releasing hormone (CRH), arginine vasopressin (AVP), and corticosterone (CORT) during this time period. Thus, the primary goal of this study was to determine whether these observed changes in important central regulators of the stress response were permanent or transient. In this study, juvenile male Wistar rats were treated with a binge-pattern EtOH treatment paradigm or saline alone for 8 days. The animals were left undisturbed until adulthood when they received a second round of treatments consisting of saline alone, a single dose of EtOH, or a second binge-pattern treatment paradigm. The results showed that pubertal binge-pattern EtOH exposure induced striking long-lasting alterations of many HPA axis parameters. Overall, our data provide strong evidence that binge-pattern EtOH exposure during pubertal maturation has long-term detrimental effects for the healthy development of the HPA axis.

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Reversal of the hypothalamo-pituitary–adrenal response to oestrogens around puberty

Cited by 27 publications

References 37 publications

Cholesterol and perhaps estradiol protect against corticosterone-induced hippocampal CA3 dendritic retraction in gonadectomized female and male rats

Cholesterol and perhaps estradiol protect against corticosterone-induced hippocampal CA3 dendritic retraction in gonadectomized female and male rats

Emergence of sex differences in the development of substance use and abuse during adolescence

Binge-Pattern Alcohol Exposure during Puberty Induces Long-Term Changes in HPA Axis Reactivity

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