Oxytocin (
Dehydroepiandrosterone (
- 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
More Like this
-
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. -
Social context often has profound effects on behavior, yet the neural and molecular mechanisms which mediate flexible behavioral responses to different social environments are not well understood. We used the African cichlid fish,
Astatotilapia burtoni , to examine aggressive defense behavior across three social contexts representing different motivational states: a reproductive opportunity, a familiar male and a neutral context. To elucidate how differences in behavior across contexts may be mediated by neural gene expression, we examined gene expression in the preoptic area, a brain region known to control male aggressive and sexual behavior. We show that social context has broad effects on preoptic gene expression. Specifically, we found that the expression of genes encoding nonapeptides and sex steroid receptors are upregulated in the familiar male context. Furthermore, circulating levels of testosterone and cortisol varied markedly depending on social context. We also manipulated the D2 receptor (D2R) in each social context, given that it has been implicated in mediating context‐dependent behavior. We found that aD2R agonist reduced intruder‐directed aggression in the reproductive opportunity and familiar male contexts, while aD2R antagonist inhibited intruder‐directed aggression in the reproductive opportunity context and increased aggression in the neutral context. Our results demonstrate a critical role for preoptic gene expression, as well as circulating steroid hormone levels, in encoding information from the social environment and in shaping adaptive behavior. In addition, they provide further evidence for a role ofD2R in context‐dependent behavior. -
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. -
Summary Auxin is widely involved in plant growth and development. However, the molecular mechanism on how auxin carries out this work is unclear. In particular, the effect of auxin on pre‐
mRNA post‐transcriptional regulation is mostly unknown. By using a poly(A) tag (PAT ) sequencing approach,mRNA alternative polyadenylation (APA ) profiles after auxin treatment were revealed. We showed that hundreds of poly(A) site clusters (PAC s) are affected by auxin at the transcriptome level, where auxin reducesPAC distribution in 5′‐untranslated region (UTR ), but increases in the 3′UTR .APA site usage frequencies of 42 genes were switched by auxin, suggesting that auxin affects the choice of poly(A) sites. Furthermore, poly(A) signal selection was altered after auxin treatment. For example, a mutant of poly(A) signal binding proteinCPSF 30 showed altered sensitivity to auxin treatment, indicating interactions between auxin and the poly(A) signal recognition machinery. We also found that auxin activity on lateral root development is likely mediated by altered expression of ,ARF 7 andARF 19 through poly(A) site switches. Our results shed light on the molecular mechanisms of auxin responses relative to its interactions withIAA 14mRNA polyadenylation. -
Abstract Objective Previously, we found that diet‐induced
HH cy in mice caused decreasedeNOS expression and signaling in mesenteric arteries, but greatly enhanced non‐NOS , non‐prostacyclin‐dependent vasodilation, which involvesMEJ communication. To further assess whetherHH cy enhancesMEJ communication, this study examined endothelium‐dependent attenuation of phenylephrine‐induced vasoconstriction (myoendothelial feedback) and key molecules involved.Methods Myoendothelial feedback was examined in isolated mouse mesenteric arteries, after 6‐weeks diet‐induced
HH cy, using pressure myography. Gap junction (Cx37, Cx40, Cx43),NOS (eNOS ,nNOS ,iNOS ), and potassium channel (IK 1) protein expression were measured with immunoblots, and connexinmRNA s with real‐timePCR . Contribution ofnNOS +iNOS to vasomotor responses was assessed using the drug TRIM.Results Myoendothelial feedback was significantly (
P < .05) enhanced inHH cy arteries compared to control, coincident with significantly greater Cx37 andIK 1 protein and Cx37mRNA . Cx43 protein, but notmRNA , was significantly less inHH cy, and Cx40 was not different.eNOS protein was significantly less inHH cy.nNOS andiNOS were not different.TRIM had little effect on vasomotor function.Conclusions Diet‐induced
HH cy enhanced myoendothelial feedback, and increased Cx37 andIK 1 expression may contribute.nNOS oriNOS did not upregulate to compensate for decreasedeNOS , and they had little involvement in vasomotor function.