Oxytocin (
Dehydroepiandrosterone (
- NSF-PAR ID:
- 10197740
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Journal of Neuroendocrinology
- Volume:
- 28
- Issue:
- 12
- ISSN:
- 0953-8194
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract OT ) often regulates social behaviours in sex‐specific ways, and this may be a result of sex differences in the brainOT system. Adult male rats show higherOT receptor (OTR ) binding in the posterior bed nucleus of the stria terminalis (pBNST ) than adult female rats. In the present study, we investigated the mechanisms that lead to this sex difference. First, we found that male rats have higherOTR mRNA expression in thepBNST than females at postnatal day (P) 35 and P60, which demonstrates the presence of the sex difference inOTR binding density at message level. Second, the sex difference inOTR binding density in thepBNST was absent at P0 and P3, but was present by P5. Third, systemic administration of the oestrogen receptor (ER ) antagonist fulvestrant at P0 and P1 dose‐dependently reducedOTR binding density in thepBNST of 5‐week‐old male rats, but did not eliminate the sex difference inOTR binding density. Fourth,pBNST ‐OTR binding density was lower in androgen receptor (AR ) deficient genetic male rats compared to wild‐type males, but higher compared to wild‐type females. Finally, systemic administration of the histone deacetylase inhibitor valproic acid at P0 and P1 did not alterpBNST ‐OTR binding density in 5‐week‐old male and female rats. Interestingly, neonatalER antagonism,AR deficiency, and neonatal valproic acid treatment each eliminated the sex difference inpBNST size. Overall, we demonstrate a role for neonatalER andAR activation in setting up the sex difference inOTR binding density in thepBNST , which may underlie sexual differentiation of thepBNST and social behaviour. -
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Abstract Many animal species exhibit year‐round aggression, a behaviour that allows individuals to compete for limited resources in their environment (eg, food and mates). Interestingly, this high degree of territoriality persists during the non‐breeding season, despite low levels of circulating gonadal steroids (ie, testosterone [T] and oestradiol [E2]). Our previous work suggests that the pineal hormone melatonin mediates a ‘seasonal switch’ from gonadal to adrenal regulation of aggression in Siberian hamsters (
Phodopus sungorus ); solitary, seasonally breeding mammals that display increased aggression during the short, ‘winter‐like’ days (SDs) of the non‐breeding season. To test the hypothesis that melatonin elevates non‐breeding aggression by increasing circulating and neural steroid metabolism, we housed female hamsters in long days (LDs) or SDs, administered them timed or mis‐timed melatonin injections (mimic or do not mimic a SD‐like signal, respectively), and measured aggression, circulating hormone profiles and aromatase (ARO) immunoreactivity in brain regions associated with aggressive or reproductive behaviours (paraventricular hypothalamic nucleus [PVN], periaqueductal gray [PAG] and ventral tegmental area [VTA]). Females that were responsive to SD photoperiods (SD‐R) and LD females given timed melatonin injections (Mel‐T) exhibited gonadal regression and reduced circulating E2, but increased aggression and circulating dehydroepiandrosterone (DHEA). Furthermore, aggressive challenges differentially altered circulating hormone profiles across seasonal phenotypes; reproductively inactive females (ie, SD‐R and Mel‐T females) reduced circulating DHEA and T, but increased E2after an aggressive interaction, whereas reproductively active females (ie, LD females, SD non‐responder females and LD females given mis‐timed melatonin injections) solely increased circulating E2. Although no differences in neural ARO abundance were observed, LD and SD‐R females showed distinct associations between ARO cell density and aggressive behaviour in the PVN, PAG and VTA. Taken together, these results suggest that melatonin increases non‐breeding aggression by elevating circulating steroid metabolism after an aggressive encounter and by regulating behaviourally relevant neural circuits in a region‐specific manner. -
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Abstract Melatonin plays a central role in entraining activity to the day–night cycle in vertebrates. Here, we investigate neuroanatomical substrates of melatonin‐dependent vocal–acoustic behavior in the nocturnal and highly vocal teleost fish, the plainfin midshipman (
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Abstract There is mounting evidence that, across taxa, females breeding in competitive environments tend to allocate more testosterone to their offspring prenatally and these offspring typically have more aggressive and faster‐growing phenotypes. To date, no study has determined the mechanisms mediating this maternal effect's influence on offspring phenotype. However, levels of estrogen receptor alpha (
ER α ) gene expression are linked to differences in early growth and aggression; thus, maternal hormones may alter gene regulation, perhaps viaDNA methylation, ofER α in offspring during prenatal development. We performed a pilot study to examine natural variation in testosterone allocation to offspring through egg yolks in wild Eastern Bluebirds (Sialia sialis ) in varying breeding densities and percentDNA methylation ofCG dinucleotides in theER α promoter in offspring brain regions associated with growth and behavior. We hypothesized that breeding density would be positively correlated with yolk testosterone, and prenatal exposure to maternal‐derived yolk testosterone would be associated with greater offspring growth and decreasedER α promoter methylation. Yolk testosterone concentration was positively correlated with breeding density, nestling growth rate, and percentDNA methylation of one out of five investigated CpG sites (site 3) in the diencephalonER α promoter, but none in the telencephalon (n = 10). PercentDNA methylation of diencephalon CpG site 3 was positively correlated with growth rate. These data suggest a possible role for epigenetics in mediating the effects of the maternal environment on offspring phenotype. Experimentally examining this mechanism with a larger sample size in future studies may help elucidate a prominent way in which animals respond to their environment. Further, by determining the mechanisms that mediate maternal effects, we can begin to understand the potential for the heritability of these mechanisms and the impact that maternal effects are capable of producing at an evolutionary scale.
