Effects of blocking developmental cell death on sexually dimorphic calbindin cell groups in the preoptic area and bed nucleus of the stria terminalis

Gilmore, Richard F; Varnum, M. M.; Forger, Nancy G.

doi:10.1186/2042-6410-3-5

Cited by 61 publications

(57 citation statements)

References 53 publications

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“…E 2 , derived from the neural aromatization of testosterone, acts perinatally to masculinize this neuronal population resulting in more cells in males than in females (Gilmore et al 2012). Developmental exposure to BPA had no effect on this cluster in the medial preoptic area as no difference in the number of calbindin immunoreactive cells was found between vehicle and BPA-exposed females ( Fig.…”

Section: Developmental Exposure To Bpa Did Not Masculinize the Femalementioning

confidence: 93%

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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Bisphenol A (BPA) is a widespread estrogenic compound. We investigated the effects of maternal exposure to BPA at reference doses on sexual behavior and neuroendocrine functions of female offspring in C57BL/6J mice. The dams were orally exposed to vehicle alone or vehicle-containing BPA at doses equivalent to the no observed adverse effect level (5 mg/kg body weight per day) and tolerable daily intake (TDI, 0.05 mg/kg body weight per day) level from gestational day 15 until weaning. Developmental exposure to BPA increased the lordosis quotient in naive females exposed to BPA at the TDI dose only. BPA exposure had no effect on olfactory preference, ability to express masculine behaviors or number of calbindin-positive cells, a sexually dimorphic population of the preoptic area. BPA at both doses selectively increased kisspeptin cell number in the preoptic periventricular nucleus of the rostral periventricular area of the third ventricle in adult females. It did not affect the number of GNRH-positive cells or percentage of kisspeptin appositions on GNRH neurons in the preoptic area. These changes were associated with higher levels of estradiol (E 2 ) at the TDI dose while levels of LH, estrus cyclicity, ovarian and uterine weights, and fertility remained unaffected. Delay in the time of vaginal opening was observed during the postnatal period at TDI dose, without any alteration in body growth. This shows that developmental exposure to BPA at reference doses did not masculinize and defeminize the neural circuitry underlying sexual behavior in female mice. The TDI dose specifically exacerbated responses normally induced by ovarian E 2 , through estrogen receptor a, during the postnatal/prepubertal period.

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Section: Developmental Exposure To Bpa Did Not Masculinize the Femalementioning

confidence: 93%

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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“…Recent data from our laboratory suggest that such effects even vary by dependent measure within a brain region. For example, in the mPOA of mice, males have more cells expressing the calcium-binding protein calbindin, but females have more cells expressing oestrogen receptor a [42,43]. We treated newborn mice, icv, with the DNMT inhibitor zebularine or vehicle, and examined effects on expression of these two proteins after weaning.…”

Section: Do the Studies To Date Contradict Each Other?mentioning

confidence: 99%

Epigenetic mechanisms in sexual differentiation of the brain and behaviour

Forger¹

2016

Phil. Trans. R. Soc. B

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One contribution of 16 to a theme issue 'Multifaceted origins of sex differences in the brain'.Subject Areas: behaviour, developmental biology, genetics, neuroscience Keywords:DNA methylation, histone, medial preoptic area, bed nucleus of the stria terminalis, sex difference Author for correspondence: Nancy G. Forger e-mail: nforger@gsu.edu Epigenetic mechanisms in sexual differentiation of the brain and behaviour Nancy G. Forger Neuroscience Institute, Georgia State University, Atlanta, GA 30307, USA Circumstantial evidence alone argues that the establishment and maintenance of sex differences in the brain depend on epigenetic modifications of chromatin structure. More direct evidence has recently been obtained from two types of studies: those manipulating a particular epigenetic mechanism, and those examining the genome-wide distribution of specific epigenetic marks. The manipulation of histone acetylation or DNA methylation disrupts the development of several neural sex differences in rodents. Taken together, however, the evidence suggests there is unlikely to be a simple formula for masculine or feminine development of the brain and behaviour; instead, underlying epigenetic mechanisms may vary by brain region or even by dependent variable within a region. Whole-genome studies related to sex differences in the brain have only very recently been reported, but suggest that males and females may use different combinations of epigenetic modifications to control gene expression, even in cases where gene expression does not differ between the sexes. Finally, recent findings are discussed that are likely to direct future studies on the role of epigenetic mechanisms in sexual differentiation of the brain and behaviour.

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“…For example, the amygdala, the intermediate nucleus of the hypothalamus, the bed nucleus of the stria terminalis (BnST), and the human homologue of the medial preoptic area, INAH1, are larger in men than in women, while prefrontal cortices are larger in women than in men (Goldstein et al, 2001; Hamann 2005; Bao and Swaab, 2011). In rodents, it has been well demonstrated that early organizational actions of sex steroids result in sex-specific differences in cell number and critical chemical signaling pathways in these same regions, suggesting that by adolescence, the neural templates that give rise to anxiety are explicitly different in the male versus the female brain (Toufexis, 2007; Forger, 2009; Harada et al, 2009; Hisasue et al, 2010; Bangasser and Valentino, 2012; Gilmore et al, 2012; Valentino et al, 2012, 2013). …”

Section: Introductionmentioning

confidence: 99%

Sex and exercise interact to alter the expression of anabolic androgenic steroid-induced anxiety-like behaviors in the mouse

Onakomaiya

Porter

Oberlander

et al. 2014

Hormones and Behavior

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Anabolic androgenic steroids (AAS) are taken by both sexes to enhance athletic performance and body image, nearly always in conjunction with an exercise regime. Although taken to improve physical attributes, chronic AAS use can promote negative behavior, including anxiety. Few studies have directly compared the impact of AAS use in males versus females or assessed the interaction of exercise and AAS. We show that AAS increase anxiety-like behaviors in female but not male mice and that voluntary exercise accentuates these sex-specific differences. We also show that levels of the anxiogenic peptide corticotrophin releasing factor (CRF) are significantly greater in males, but that AAS selectively increase CRF levels in females, thus abrogating this sex-specific difference. Exercise did not ameliorate AAS-induced anxiety or alter CRF levels in females. Exercise was anxiolytic in males, but this behavioral outcome did not correlate with CRF levels. Brain-derived neurotrophic factor (BDNF) has also been implicated in the expression of anxiety. As with CRF, levels of hippocampal BDNF mRNA were significantly greater in males than females. AAS and exercise were without effect on BDNF mRNA in females. In males, anxiolytic effects of exercise correlated with increased BDNF mRNA, however AAS-induced changes in BDNF mRNA and anxiety did not. In sum, we find that AAS elicit sex-specific differences in anxiety and that voluntary exercise accentuates these differences. In addition, our data suggest that these behavioral outcomes may reflect convergent actions of AAS and exercise on a sexually differentiated CRF signaling system within the extended amygdala.

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Effects of blocking developmental cell death on sexually dimorphic calbindin cell groups in the preoptic area and bed nucleus of the stria terminalis

Cited by 61 publications

References 53 publications

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Epigenetic mechanisms in sexual differentiation of the brain and behaviour

Sex and exercise interact to alter the expression of anabolic androgenic steroid-induced anxiety-like behaviors in the mouse

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