Development of sex differences in the principal nucleus of the bed nucleus of the stria terminalis of mice: Role ofBax-dependent cell death

2007 ◽  
Vol 67 (3) ◽  
pp. 355-362 ◽  
Author(s):  
Tina Gotsiridze ◽  
Ningdong Kang ◽  
Dena Jacob ◽  
Nancy G. Forger
Keyword(s):  
Cell Death ◽  
Sex Differences ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Dependent Cell

scholarly journals Epigenetic Control of Sexual Differentiation of the Bed Nucleus of the Stria Terminalis

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4241-4247 ◽  
Author(s):  
Elaine K. Murray ◽  
Annie Hien ◽  
Geert J. de Vries ◽  
Nancy G. Forger
Keyword(s):  
Cell Death ◽  
Sex Differences ◽  
Sexual Differentiation ◽  
Cell Number ◽  
Histone Deacetylation ◽  
Postnatal Life ◽  
Sexually Dimorphic ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Deacetylase Inhibitor

Abstract The principal nucleus of the bed nucleus of the stria terminalis (BNSTp) is larger in volume and contains more cells in male than female mice. These sex differences depend on testosterone and arise from a higher rate of cell death during early postnatal life in females. There is a delay of several days between the testosterone surge at birth and sexually dimorphic cell death in the BNSTp, suggesting that epigenetic mechanisms may be involved. We tested the hypothesis that chromatin remodeling plays a role in sexual differentiation of the BNSTp by manipulating the balance between histone acetylation and deacetylation using a histone deacetylase inhibitor. In the first experiment, a single injection of valproic acid (VPA) on the day of birth increased acetylation of histone H3 in the brain 24 h later. Next, males, females, and females treated neonatally with testosterone were administered VPA or saline on postnatal d 1 and 2 and killed at 21 d of age. VPA treatment did not influence volume or cell number of the BNSTp in control females but significantly reduced both parameters in males and testosterone-treated females. As a result, the sex differences were eliminated. VPA did not affect volume or cell number in the suprachiasmatic nucleus or the anterodorsal nucleus of the thalamus, which also did not differ between males and females. These findings suggest that a disruption in histone deacetylation may lead to long-term alterations in gene expression that block the masculinizing actions of testosterone in the BNSTp.

scholarly journals Regulation of CRF mRNA in the Rat Extended Amygdala Following Chronic Cocaine: Sex Differences and Effect of Delta Opioid Receptor Agonism

2019 ◽  
Vol 23 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Krista L Connelly ◽  
Ellen M Unterwald
Keyword(s):  
Sex Differences ◽  
Opioid Receptor ◽  
Receptor Agonist ◽  
Female Rats ◽  
Delta Opioid Receptor ◽  
Stria Terminalis ◽  
Central Amygdala ◽  
Cocaine Withdrawal ◽  
Bed Nucleus ◽  
Opioid Receptor Agonist

Abstract Background Cocaine withdrawal activates stress systems. Females are more vulnerable to relapse to cocaine use and more sensitive to withdrawal-induced negative affect. Delta opioid receptors modulate anxiety-like behavior during cocaine withdrawal in rats. This study measured the time course of gene regulation of one of the main stress peptides, corticotropin-releasing factor (CRF), and its type 1 receptor in male and female rats as well as the ability of the delta opioid receptor agonist SNC80 to normalize cocaine withdrawal-induced changes in CRF mRNA. Methods Rats were injected with cocaine or saline 3 times daily for 14 days. Brains were collected 30 minutes, 24 hours, 48 hours, 7 days, and 14 days following the last injection. The paraventricular nucleus of the hypothalamus, central amygdala, and bed nucleus of the stria terminalis were processed for quantitative reverse transcriptase PCR measurement of CRF and CRFR1 mRNA. Additional rats received SNC80 during early cocaine withdrawal, and CRF mRNA was measured in the central amygdala. Results CRF mRNA was elevated in the central amygdala at 24 hours and the paraventricular nucleus at 48 hours of cocaine withdrawal in males and females. Significant sex differences in cocaine-induced CRF upregulation were found in the bed nucleus of the stria terminalis at 30 minutes and 24 hours. SNC80 administration attenuated the increase in CRF mRNA in the central amygdala of female rats only. Conclusions CRF mRNA regulation during cocaine withdrawal is sex, time, and brain region dependent. Administration of a delta opioid receptor agonist during early withdrawal may ameliorate stress-related negative affect in females by abrogating the induction of CRF mRNA.

scholarly journals Neonatal Inhibition of DNA Methylation Disrupts Testosterone-Dependent Masculinization of Neurochemical Phenotype

Endocrinology ◽  
2019 ◽  
Vol 161 (1) ◽  
Author(s):  
Carla D Cisternas ◽  
Laura R Cortes ◽  
Ilona Golynker ◽  
Alexandra Castillo-Ruiz ◽  
Nancy G Forger
Keyword(s):  
Dna Methylation ◽  
Sex Differences ◽  
Estrogen Receptor Alpha ◽  
Molecular Mechanisms ◽  
Preoptic Area ◽  
Cell Types ◽  
Cell Number ◽  
Cell Phenotype ◽  
Stria Terminalis ◽  
Bed Nucleus

Abstract Many neural sex differences are differences in the number of neurons of a particular phenotype. For example, male rodents have more calbindin-expressing neurons in the medial preoptic area (mPOA) and bed nucleus of the stria terminalis (BNST), and females have more neurons expressing estrogen receptor alpha (ERα) and kisspeptin in the ventromedial nucleus of the hypothalamus (VMH) and the anteroventral periventricular nucleus (AVPV), respectively. These sex differences depend on neonatal exposure to testosterone, but the underlying molecular mechanisms are unknown. DNA methylation is important for cell phenotype differentiation throughout the developing organism. We hypothesized that testosterone causes sex differences in neurochemical phenotype via changes in DNA methylation, and tested this by inhibiting DNA methylation neonatally in male and female mice, and in females given a masculinizing dose of testosterone. Neonatal testosterone treatment masculinized calbindin, ERα and kisspeptin cell number of females at weaning. Inhibiting DNA methylation with zebularine increased calbindin cell number only in control females, thus eliminating sex differences in calbindin in the mPOA and BNST. Zebularine also reduced the sex difference in ERα cell number in the VMH, in this case by increasing ERα neuron number in males and testosterone-treated females. In contrast, the neonatal inhibition of DNA methylation had no effect on kisspeptin cell number. We conclude that testosterone normally increases the number of calbindin cells and reduces ERα cells in males through orchestrated changes in DNA methylation, contributing to, or causing, the sex differences in both cell types.

scholarly journals Sex differences in the Role of Basolateral Amygdala Projections to the Bed Nucleus of the Stria Terminalis in Anticipatory Anxiety

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Jaime Vantrease ◽  
Brittany Avonts ◽  
Mary DeJoseph ◽  
Janice Urban ◽  
Jeremy Rosenkranz
Keyword(s):  
Sex Differences ◽  
Basolateral Amygdala ◽  
Stria Terminalis ◽  
Anticipatory Anxiety ◽  
Bed Nucleus
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