Hormones and Behavior最新文献

Vasopressin (AVP) regulates various social behaviors, often in sex-specific ways, including social play behavior, a rewarding behavior displayed primarily by juveniles. Here, we examined whether and how AVP acting in the brain's reward system regulates social play behavior in juvenile rats. Specifically, we focused on AVP signaling in the ventral pallidum (VP), a brain region that is a part of the reward system. First, we examined the organization of the VP-AVP system in juvenile rats and found sex differences, with higher density of both AVP-immunoreactive fibers and AVP V1a receptor (V1aR) binding in males compared to females while females show a greater number of V1aR-expressing cells compared to males. We further found that, in both sexes, V1aR-expressing cells co-express a GABA marker to a much greater extent (approx. 10 times) than a marker for glutamate. Next, we examined the functional involvement of V1aR-expressing VP cells in social play behavior. We found that exposure to social play enhanced the proportion of activated V1aR-expressing VP cells in males only. Finally, we showed that infusion of a specific V1aR antagonist into the VP increased social play behaviors in juvenile male rats while decreasing these behaviors in juvenile female rats. Overall, these findings reveal structural and functional sex differences in the AVP-V1aR system in the VP that are associated with the sex-specific regulation of social play behavior.

Offspring from females breeding in competitive social environments are often exposed to more testosterone (T) during embryonic development, which can affect traits from growth to behavior in potentially adaptive ways. Despite the important role of maternally derived steroids in shaping offspring development, the molecular mechanisms driving these processes are currently unclear. Here, we use tree swallows (Tachycineta bicolor) to explore the effects of the maternal social environment on yolk T concentrations and genome-wide patterns of neural gene expression in embryos. We measured aggressive interactions among females breeding at variable densities and collected their eggs at two timepoints, including the day laid to measure yolk T concentrations and on embryonic day 11 to measure gene expression in whole brain samples. We found that females breeding in high-density sites experienced elevated rates of physical aggression and their eggs had higher yolk T concentrations. A differential gene expression and weighted gene co-expression network analysis indicated that embryos from high-density sites experienced an upregulation of genes involved in hormone, circulatory, and immune processes, and these gene expression patterns were correlated with yolk T levels and aggression. Genes implicated in neural development were additionally downregulated in embryos from high-density sites. These data highlight how early neurogenomic processes may be affected by the maternal social environment, giving rise to phenotypic plasticity in offspring.

Previous studies support links among maternal-fetal attachment, psychological symptoms, and hormones during pregnancy and the post-partum period. Other studies connect maternal feelings and behaviors to oxytocin and suggest that an increase in oxytocin during pregnancy may prime maternal-fetal attachment. To date, researchers have not examined a possible association between maternal-fetal attachment with human placental lactogen although animal models are suggestive. In the current study, we sought to describe oxytocin and human placental lactogen levels as related to psychological constructs across pregnancy. Seventy women participated in the study. At each of three time-points (early, mid, and late pregnancy), the women had their blood drawn to assess oxytocin and human placental lactogen levels, and they completed psychological assessments measuring maternal-fetal attachment, anxiety, and depression. Our results indicate that oxytocin levels were statistically similar across pregnancy, but that human placental lactogen significantly increased across pregnancy. Results did not indicate significant associations of within-person (comparing individuals to themselves) oxytocin or human placental lactogen levels with maternal-fetal attachment. Additionally, results did not show between-person (comparing individuals to other individuals) oxytocin or human placental lactogen levels with maternal-fetal attachment. Oxytocin levels were not associated with anxiety; rather the stage of pregnancy moderated the effect of the within-person OT level on depression. Notably, increasing levels of human placental lactogen were significantly associated with increasing levels of both anxiety and depression in between subject analyses. The current study is important because it describes typical hormonal and maternal fetal attachment levels during each stage of pregnancy, and because it suggests an association between human placental lactogen and psychological symptoms during pregnancy. Future research should further elucidate these relationships.

Alamandine is a peptide hormone belonging to the renin–angiotensin system (RAS). It acts through the Mas-related G-protein coupled receptor type D, MrgD, which is expressed in different tissues, including the brain. In the present study, we hypothesize that a lack of alamandine, through MrgD, could cause the anxiety-like behavior in transgenic rats with low brain angiotensinogen [TGR(ASrAOGEN)680]. Adult male transgenic rats exhibited a significant increase in the latency to feeding time in the novelty suppressed feeding test and a decrease in the percentage of time and entries in the open arms in the elevated plus maze. These effects were reversed by intracerebroventricular infusion of alamandine. Pretreatment with D-Pro⁷-Ang-(1–7), a Mas and MrgD receptor antagonist, prevented the anxiolytic effects induced by this peptide. However, its effects were not altered by the selective Mas receptor antagonist, A779. In conclusion, our data indicates that alamandine, through MrgD, attenuates anxiety-like behavior in male TGR(ASrAOGEN)680, which reinforces the importance of the counter-regulatory RAS axis as promising target for the treatment of neuropsychiatric disorders.

The ability of individual animals to defend a territory as well as various phenotypic and behavioral traits may be targets of sexual selection used by males to evaluate their competitors or by females to choose males. A frequent question in animal behavior is whether male traits and characteristics of their territory are correlated and what are the mechanisms that may mediate such associations when they exist. Because hormones link phenotype to behavior, by studying the role of testosterone in territoriality one may come closer to understanding the mechanisms mediating correlations or lack thereof between characteristics of territories and of males. We evaluated whether variation in characteristics of territories (size and quality) are correlated with variation in morphology, coloration, testosterone, heterozygosity, and calls in two species of poison frogs. The Amazonian frog Allobates aff. trilineatus exhibits male care and defends territories only during the breeding season, while the endangered frog Oophaga lehmanni displays maternal care and defends territories throughout the year. We found that morphological traits (body length, weight, thigh size), call activity, and testosterone levels correlated with size and various indicators of quality of the territory. However, the direction of these correlations (whether positive or negative) and which specific morphological, acoustic traits or testosterone level variables covaried depended on the species. Our findings highlight an endocrine pathway as part of the physiological machinery that may underlie the interplay between male traits and territorial behavior. We were able to identify some male traits related to territory attributes, but whether females choose males based on these traits requires further research.

The synthetic progestin, 17α-hydroxyprogesterone caproate (17-OHPC), is administered to pregnant individuals at risk for preterm birth and is likely transferred from mother to fetus. Yet, there is little information regarding the potential effects of 17-OHPC administration on behavioral and neural development in offspring. In rats, neonatal 17-OHPC exposure altered dopaminergic fiber distribution and density in the prelimbic medial prefrontal cortex (mPFC) in neonates and adolescents, respectively. Additionally, neonatal 17-OHPC exposure in male rats increased response omissions in a delay discounting task of impulsive decision-making. Because developmental 17-OHPC exposure has differential effects in males and females, investigating the effects of 17-OHPC on impulsive decision-making in female rats is necessary. The present study tested the effects of developmental 17-OHPC exposure (P1–P14) in a delay discounting task in which female rats chose between a small immediate reward and a larger delayed (0, 15 30, or 45 s) reward. 17-OHPC-exposed females made more omissions than controls. There was no effect of 17-OHPC on large reward preference nor on response time, and omissions were similar during both free- and forced-choice trials. The present study also aimed to investigate the neural mechanisms underlying omissions in 17-OHPC-exposed female rats. The dopamine transporter inhibitor, methylphenidate (MPH), was administered prior to delay discounting testing. MPH treatment did not reduce omissions in 17-OHPC-exposed females. If anything, MPH increased omissions in control females nearly fourfold during the longest delays. These results suggest that developmental 17-OHPC exposure increased omissions without affecting impulsivity or slowing decision-making. Furthermore, omissions may be regulated, at least in part, by dopaminergic mechanisms.

The peptide hormone prolactin plays an important role in the expression of parental care behaviours across bird and mammal taxa. While a great deal is known about how plasma prolactin concentrations vary across the reproductive cycle, the few studies that investigate how prolactin relates to individual-level variation in parental care have reported mixed results. We argue that, since parental care is also affected by social interactions and environmental constraints, prolactin may better reflect behaviours that are indirectly related to parenting than the absolute level of care that is eventually expressed. In this study, we tested for associations between plasma prolactin and the expression of both parental care and proximity to the partner in incubating black-headed gulls, Chroicocephalus ridibundus. Baseline prolactin levels increased with calendar date but were unrelated to incubation behaviours. However, parents who showed a weaker decrease in prolactin to an acute stressor spent more time in close proximity to their incubating partner while not on the nest themselves, suggesting that individual variation in stress-induced prolactin changes reflect differences in parents' tendency to be closely associated with their partner and the joint nesting attempt. Baseline and stress-induced levels of the stress hormone corticosterone were unrelated to both prolactin levels and parental behaviours, suggesting that this hormone is not a strong moderator of parental care in black-headed gulls. One potential explanation for the link between prolactin dynamics and partner proximity is that prolactin reflects parental motivation to provide parental care or retain contact with the breeding partner, but further work is needed to directly test this hypothesis.

Sex/gender differences in personality associated with gender stereotyped behavior are widely studied in psychology yet remain a subject of ongoing debate. Exposure to testosterone during developmental periods is considered to be a primary mediator of many sex/gender differences in behavior. Extensions of this research has led to both lay beliefs and initial research about individual differences in basal testosterone in adulthood relating to “masculine” personality. In this study, we explored the relationships between testosterone, gender identity, and gender stereotyped personality attributes in a sample of over 400 university students (65 % female assigned at birth). Participants provided ratings of their self-perceived masculinity and femininity, resulting in a continuous measure of gender identity, and a set of agentic and communal personality attributes. A saliva sample was also provided for assay of basal testosterone. Results showed no compelling evidence that basal testosterone correlates with gender-stereotyped personality attributes or explains the relationship between sex/gender identity and these attributes, across, within, or covarying out sex assigned at birth. Contributing to a more gender diverse approach to assessing sex/gender relationships with personality and testosterone, our continuous measure of self-perceived masculinity and femininity predicted additional variance in personality beyond binary sex and showed some preliminary but weak relationships with testosterone. Results from this study cast doubt on the activational testosterone-masculinity hypothesis for explaining sex differences in gender stereotyped traits and within-sex/gender variation in attributes associated with agency and communality.

Essentially all neuropsychiatric diagnoses show some degree of sex and/or gender differences in their etiology, diagnosis, or prognosis. As a result, the roles of sex-related variables in behavior and cognition are of strong interest to many, with several lines of research showing effects on executive functions and value-based decision making in particular. These findings are often framed within a sex binary, with behavior of females described as less optimal than male “defaults”-- a framing that pits males and females against each other and deemphasizes the enormous overlap in fundamental neural mechanisms across sexes. Here, we propose an alternative framework in which sex-related factors encompass just one subset of many sources of valuable diversity in cognition. First, we review literature establishing multidimensional, nonbinary impacts of factors related to sex chromosomes and endocrine mechanisms on cognition, focusing on value- based decision-making tasks. Next, we present two suggestions for nonbinary interpretations and analyses of sex-related data that can be implemented by behavioral neuroscientists without devoting laboratory resources to delving into mechanisms underlying sex differences. We recommend (1) shifting interpretations of behavior away from performance metrics and towards strategy assessments to avoid the fallacy that the performance of one sex is worse than another; and (2) asking how much variance sex explains in measures and whether any differences are mosaic rather than binary, to avoid assuming that sex differences in separate measures are inextricably correlated. Nonbinary frameworks in research on cognition will allow neuroscience to represent the full spectrum of brains and behaviors.