Anabolic-Androgenic Steroid Effects on Sexual Receptivity in Ovariectomized Rats

Blasberg, Meg E.; Clark, Ann S.

doi:10.1006/hbeh.1997.1422

Cited by 27 publications

(16 citation statements)

References 51 publications

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“…This result is similar to those of previous experiments, where the treatment of ovariectomized prepubertal rats with aromatizable androgens advanced VO, ruling out an effect dependent on the function of the ovary [22][23][24]. In other experiments conducted in our laboratory, systemic administration of stanozolol induced central effects, as evidenced by changes in behavior [25,26]. We hypothesize that the lack of central action of stanozolol in the present study is due to the limited time course (a single injection) of stanozolol administration, the weak affinity of stanozolol for the ER, or some combination of these factors.…”

Section: Mechanism and Site Of Actionsupporting

confidence: 93%

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

Whitney¹,

Clark²

2001

Biology of Reproduction

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The effects of anabolic-androgenic steroid (AAS) abuse on the onset of puberty in female adolescents are largely unknown. This study assessed the acute effects of one AAS, stanozolol, on pubertal onset in the female rat. A single injection of stanozolol (5 mg/kg) on Postnatal Day (PN) 21 advanced vaginal opening but did not alter the onset of vaginal estrus. Higher doses of stanozolol treatment (10 and 25 mg/kg) also advanced vaginal opening but had no effect on vaginal estrus. The advancement of vaginal opening by stanozolol (5 mg/kg) was prevented by the concomitant administration of the pure antiestrogen ICI 182,780 (1 mg/kg) on PN20-22. Administration of the androgen receptor antagonist flutamide (10 mg/kg twice daily) on PN20-22 had no effect on the advancement of vaginal opening by stanozolol. Stanozolol treatment also advanced vaginal opening in ovariectomized rats. Perivaginal injections of a low dose of stanozolol (0.05 mg) on PN21 and PN23 also advanced vaginal opening. These results suggest that stanozolol is acting directly at estrogen receptors in the vaginal epithelium to advance vaginal opening and that prepubertal stanozolol treatment does not induce true precocious puberty.

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Section: Mechanism and Site Of Actionsupporting

confidence: 93%

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

Whitney¹,

Clark²

2001

Biology of Reproduction

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“…It is known that the estrous cycle in rats is regulated by the plasma levels of estrogen and progesterone (Kaeoket et al 2001) and that ND treatment induces constant diestrus in rats, with consequent reduction in their reproductive capacity (Gerez et al 2005;Blasberg and Clark 1997). High levels of androgens can affect gonadotropin release through a mechanism of negative feedback, this cause a reduction on estrogen levels in these animals (Bordbar et al 2014;Gerez et al 2005).…”

Section: Discussionmentioning

confidence: 96%

Nandrolone decanoate induces cardiac and renal remodeling in female rats, without modification in physiological parameters: The role of ANP system

et al. 2015

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“…Behavioral testing commenced at BPN55, and treatment with either AAS or oil was continued during testing. AAS treatment imposes an anestrous state characterized by diestras-like profiles (Blasberg and Clark, 1997;Penatti et al, 2009aPenatti et al, , 2011, and control mice were assessed in diestras (Cooper et al, 1993). In some experiments, PN55 diestras female mice that had not received any injections (naïve) were used.…”

Section: Animal Care and Usementioning

confidence: 99%

Corticotropin-Releasing Factor Modulation of Forebrain GABAergic Transmission has a Pivotal Role in the Expression of Anabolic Steroid-Induced Anxiety in the Female Mouse

Oberlander

Henderson

2012

Neuropsychopharmacol

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Increased anxiety is commonly observed in individuals who illicitly administer anabolic androgenic steroids (AAS). Behavioral effects of steroid abuse have become an increasing concern in adults and adolescents of both sexes. The dorsolateral bed nucleus of the stria terminalis (dlBnST) has a critical role in the expression of diffuse anxiety and is a key site of action for the anxiogenic neuromodulator, corticotropin releasing factor (CRF). Here we demonstrate that chronic, but not acute, exposure of female mice during adolescence to AAS augments anxiety-like behaviors; effects that were blocked by central infusion of the CRF receptor type 1 antagonist, antalarmin. AAS treatment selectively increased action potential (AP) firing in neurons of the central amygdala (CeA) that project to the dlBnST, increased the frequency of GABA(A) receptor-mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in dlBnST target neurons, and decreased both c-FOS immunoreactivity (IR) and AP frequency in these postsynaptic cells. Acute application of antalarmin abrogated the enhancement of GABAergic inhibition induced by chronic AAS exposure whereas application of CRF to brain slices of naïve mice mimicked the actions of this treatment. These results, in concert with previous data demonstrating that chronic AAS treatment results in enhanced levels of CRF mRNA in the CeA and increased CRF-IR in the dlBnST neuropil, are consistent with a mechanism in which the enhanced anxiety elicited by chronic AAS exposure involves augmented inhibitory activity of CeA afferents to the dlBnST and CRF-dependent enhancement of GABAergic inhibition in this brain region.

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Anabolic-Androgenic Steroid Effects on Sexual Receptivity in Ovariectomized Rats

Cited by 27 publications

References 51 publications

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

Nandrolone decanoate induces cardiac and renal remodeling in female rats, without modification in physiological parameters: The role of ANP system

Corticotropin-Releasing Factor Modulation of Forebrain GABAergic Transmission has a Pivotal Role in the Expression of Anabolic Steroid-Induced Anxiety in the Female Mouse

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