Many animals exhibit seasonal changes in physiology and behavior, including reproductive and non-reproductive social behaviors. Some seasonally-breeding animals display increases in territorial aggression during the shor...Many animals exhibit seasonal changes in physiology and behavior, including reproductive and non-reproductive social behaviors. Some seasonally-breeding animals display increases in territorial aggression during the short days (i.e., winter), despite gonadal regression and reduced circulating steroid hormones. Previous research suggests that melatonin acts via steroid hormones to regulate seasonal aggression in Siberian hamsters (Phodopus sungorus), a species in which males and females exhibit increased territorial aggression during the non-breeding season. Previously, we identified a role for adrenal dehydroepiandrosterone (DHEA) in regulating territorial aggression. Little is known, however, regarding potential seasonal changes in non-territorial aggression in this or other species. Here, we examined how short days and exogenous melatonin influence non-territorial and territorial aggression and explored the neuroendocrine circuits involved in regulating aggression in female hamsters. Specifically, we housed females in long (LD) or short-days (SD), administered timed melatonin (MEL) or control injections, and assessed territorial (i.e., resident-intruder) and non-territorial (i.e., neutral cage) aggression. Further, we quantified serum DHEA and neural activity in specific brain regions by c-Fos immunolabeling. SD and MEL-treated LD animals exhibited reproductive inhibition and increased territorial, but not non-territorial aggression, suggesting the neuroendocrine regulation of seasonal aggression is context-specific. Further, DHEA was elevated following behavioral challenges; c-Fos expression in specific brain regions was both context- and season-dependent. Collectively, these findings highlight the role of melatonin in coordinating a "seasonal switch" in aggression while suggesting the neuroendocrine mechanisms may differ across types of aggression.
Urbanization drastically alters environments, presenting wildlife with novel challenges to which they must adjust to persist. Often, an animal's first response to environmental change is to shift behavior, which requires...Urbanization drastically alters environments, presenting wildlife with novel challenges to which they must adjust to persist. Often, an animal's first response to environmental change is to shift behavior, which requires processing environmental cues into neural signals that can govern adaptive behavior. However, the neural mechanisms underpinning behavioral responses to urbanization are largely unresolved. During the breeding season, urban songbirds of several species are more aggressive than their rural counterparts. Among the many neural mechanisms that regulate aspects of aggression, arginine vasotocin (AVT) is a neuropeptide highly implicated in the regulation of sociality, including territorial aggression. Prior work has shown that the abundance of AVT peptide is associated with behavioral responses to urbanization. However, social behavior is also influenced by AVT receptor availability, making it important to compare receptor distribution and expression between urban and rural birds. To address this gap in understanding of how AVT receptors could contribute to behavioral responses to urbanization, we used in situ hybridization to describe the distribution of one AVT receptor known to influence behavior, AVT3R, throughout the brain of adult urban and rural male song sparrows (Melospiza melodia). Additionally, we used quantitative PCR (qPCR) to compare the relative expression of mRNA for AVTI1 (AVT), and two of its receptors (AVT3R and AVT4R) in the hypothalamus. We predicted that urban males would have a higher abundance of AVT3R transcripts in the lateral septum, greater mRNA expression of AVT receptors in the hypothalamus, and a positive correlation of AVT gene targets with aggression compared to rural males. We observed high AVT3R mRNA signal in the lateral septum, medial bed nucleus of the stria terminalis, hippocampus, nidopallium, cerebellum and optic tectum, with diffuse signal in the lateral hypothalamus and nucleus rotundus. There were no significant differences in the number of AVT3R transcripts in the lateral septum between urban and rural males. When we quantified relative mRNA expression of AVT and two of its receptors using qPCR, we found that urban males had higher relative mRNA expression of AVT3R in the hypothalamus compared to rural males, and aggression immediately before capture was negatively associated with the expression of AVT, AVT3R, and AVT4R. Thus, expression of AVT and its receptors has the potential to contribute to higher aggression in male song sparrows but may not explain habitat-related variation.
Levonorgestrel (LNG), a contraceptive hormone, is used by millions of women worldwide. We have found that LNG delays habit expression in gonadally-intact female rats, suggesting it influences cognitive processes. The mec...Levonorgestrel (LNG), a contraceptive hormone, is used by millions of women worldwide. We have found that LNG delays habit expression in gonadally-intact female rats, suggesting it influences cognitive processes. The mechanism driving LNG's effect on habit in female rats remains unclear. One explanation is that LNG's androgenic properties impact habit learning. To investigate this, intact female rats were implanted subcutaneously with either cholesterol- (Experiment 1) or LNG- (Experiment 2) capsules. Animals from each group received subcutaneous injections of flutamide, an androgen receptor antagonist, or vehicle prior to sessions of appetitive operant training. After training, half of the rats in each experimental group received outcome devaluation, which rendered the sucrose reward aversive. Subsequently, all rats underwent a short extinction test to ascertain whether behavior was goal-directed or habitual. In Experiment 1, habit was observed in cholesterol-implanted females, and this was not affected by flutamide, replicating our earlier finding that habit is present after moderate training in intact female rats, and additionally showing that blocking androgen receptor activity during training does not alter habit expression. In Experiment 2, LNG-implanted rats exhibited goal-directed behavior, again replicating our previous findings showing that LNG delays habit in female rats. However, LNG-implanted rats treated with flutamide during training displayed habitual behavior, suggesting that the androgenic effects of LNG are responsible, at least in part, for delaying habit expression in intact female rats. This finding suggests that the androgenic properties of LNG are exerting significant effects on cognitive processes related to behavioral flexibility in the female brain.
Poor sleep hygiene is reported to impair subjective sleep and disrupt circadian system, yet the association between sleep hygiene and objective alterations in sleep continuity is scarcely studied. Moreover, the role of g...Poor sleep hygiene is reported to impair subjective sleep and disrupt circadian system, yet the association between sleep hygiene and objective alterations in sleep continuity is scarcely studied. Moreover, the role of gender differences is largely neglected. In this pilot study, sixty-five adults (66% females) completed a psychometric assessment including the Sleep Hygiene Index (SHI) and wore an actigraph for one week for the assessment of sleep. No statistically significant gender differences on sleep hygiene practices were found. Bedtime and waketime were later in males than females. Males showed longer sleep onset latency (SOL), and wake after sleep onset (WASO), and lower sleep efficiency compared to females. General linear analyses showed that poorer sleep hygiene was associated with shorter SOL and longer WASO in males but not in females. Age, habitual insomnia and psychological distress did not influence the results. Current findings suggest a differential impact of sleep hygiene behaviors on objective alternations in males. While future research is needed to investigate the role of specific sleep promoting and sleep inhibiting behaviors on objective sleep, current results highlight the importance of considering gender differences in sleep hygiene research. Gender differences in homeostatic, circadian, and neuroendocrine factors related to sleep hygiene should be further investigated in mechanistic studies also considering non-binary participants.
Steroid hormones influence affective behavior and its underlying neural networks. However, distinguishing between organizational and activational hormonal effects, along with effects of socialization, remains challenging...Steroid hormones influence affective behavior and its underlying neural networks. However, distinguishing between organizational and activational hormonal effects, along with effects of socialization, remains challenging, limiting the understanding of the mechanisms underlying affective neurobehavioral differences. Individuals with differences in sex development (DSD), such as congenital adrenal hyperplasia (CAH) and complete androgen insensitivity syndrome (CAIS), offer a unique opportunity to examine how alterations in prenatal steroid hormone exposure have a role in shaping brain development and human behaviors. This review aims to examine how, and to what extent CAH and CAIS, can inform broader neuroendocrine mechanisms of affective behavior. It starts with an overview of experimental psychology and human imaging work on the role of steroid hormones in affective behavior, highlighting the main challenges in the field in human research, and the rationale for including CAH and CAIS. It then summarizes findings from behavioral studies, experimental psychology, and neuroimaging research in CAH and CAIS to discuss how this research contributes to the understanding of the organizational role of steroid hormones on affective outcomes. Although the current evidence is limited and heterogeneous, this review highlights the contribution of prenatal hormonal variability, particularly prenatal androgen exposure, in shaping affective behavior and underlying neural networks. It also highlights how steroid hormones, chromosomal sex, timing of hormonal exposure, developmental stage and psychosocial factors interact in influencing affective outcomes. Advancing this work through neuroimaging and standardized experimental paradigms has the potential to specify the mechanistic pathways through which steroid hormone variability influences behavior. This work can also inform targeted interventions and support emotional well-being and quality of life for individuals with CAH and CAIS.
The Dual Hormone Hypothesis is a biosocial model that describes the interactive effects of testosterone and cortisol on status-relevant behavior. Under this model, testosterone increases status-seeking behavior when cort...The Dual Hormone Hypothesis is a biosocial model that describes the interactive effects of testosterone and cortisol on status-relevant behavior. Under this model, testosterone increases status-seeking behavior when cortisol is low, and status-loss-avoidance when cortisol is high. This manifests as high-testosterone individuals preferentially competing against high-status opponents when cortisol is low, and low-status opponents when cortisol is high. However, opponent status indicates both potential status gain as well as opponent strength. The present study separates opponent status from potential gains and losses to understand how testosterone and cortisol interact with different status cues during competition. Results suggest that testosterone increases sensitivity to opponent status while decreasing sensitivity to gains and losses. Cortisol moderates testosterone's effects on status sensitivity while independently increasing reward sensitivity. Furthermore, the present work leverages machine learning to elucidate how testosterone influences behavior in a nonlinear fashion.
This study examined the effects of resistance training (RT) and supraphysiological nandrolone decanoate (ND) administration on hippocampal neurogenesis, neurotrophic signaling, and behavior. Forty 3-month-old male C57BL/...This study examined the effects of resistance training (RT) and supraphysiological nandrolone decanoate (ND) administration on hippocampal neurogenesis, neurotrophic signaling, and behavior. Forty 3-month-old male C57BL/6 J mice were randomized to RT or sedentary (SED) conditions. Each group was further divided into sham (S) or ND (38 mg·kg·wk.) treatment groups. All interventions lasted 7 wk. Adult hippocampal neurogenesis was quantified in the dentate gyrus using BrdU/NeuN immunolabeling. Hippocampal expression of brain-derived neurotrophic factor (BDNF), androgen receptor (AR), estrogen receptor-β (ER-β), insulin-like growth factor-1 (IGF-1), and irisin was assessed by western blot analyses. No significant exercise × treatment interactions were observed for any of the behavior measures. When collapsed across treatments, RT exhibited a greater number of open-arm entries (p = 0.006) and reduced average latency times (p = 0.002) than SED. ND administration did not alter behavioral outcomes. RT (p = 0.001) and ND (p = 0.032) each independently increased hippocampal BrdU/NeuN cell numbers, with no additive effects. AR expression for SED-S was significantly lower (p's < 0.05) than all other groups and IGF-1 expression for RT-S was significantly greater (p's < 0.05) than all other groups. Main effects revealed that RT and ND resulted in significant elevations in AR, ER-β and BDNF expressions. In conclusion, RT enhanced hippocampal plasticity and behavioral performance, whereas supraphysiological ND administration produced distinct molecular changes without conferring additive behavioral or neuroplastic benefit.
Some theories have proposed that children with autism spectrum disorder (ASD) may be exposed to increased levels of androgens during prenatal development, resulting in greater androgenization of testosterone-dependent tr...Some theories have proposed that children with autism spectrum disorder (ASD) may be exposed to increased levels of androgens during prenatal development, resulting in greater androgenization of testosterone-dependent traits including both peripheral (bodily) and central (brain-related) traits. Empirical support for this hypothesis is scant and inconsistent. In the present work, we studied an ostensible anatomical marker of testosterone exposure (sexually differentiated finger lengths) which develops during the first trimester or early second trimester of gestation. Participants were 25 boys with classic autism, recruited from the clinical practice of a local physician specializing in childhood autism, who met the standardized DSM (Diagnostic and Statistical Manual) criteria for ASD, and 57 normally-developing age- and sex-matched male and female controls (32 males, 25 females); N = 82; M = 7.30 yrs., SD = 4.18. Finger length was measured to the nearest 0.5 mm from digital images of the ventral surface of the hands using a validated measurement protocol. Consistent with past reports from adult samples, several of the finger length ratios were confirmed to display sex differences among control children, but the group of boys with ASD showed a female-like finger growth pattern, not the hypermasculine pattern predicted, and were found to differ statistically from the male controls. Boys with ASD thus showed a demasculinized pattern of finger differentiation. Our data do not support theories which suggest that greater fetal testosterone exposure occurs in boys with autism.
Aggression, a conserved social behavior, is orchestrated by a distributed neural network where sex hormone receptors integrate hormonal and experiential signals. This review synthesizes recent rodent studies, highlightin...Aggression, a conserved social behavior, is orchestrated by a distributed neural network where sex hormone receptors integrate hormonal and experiential signals. This review synthesizes recent rodent studies, highlighting the central role of estrogen receptor alpha (ERα). We delineate a striking functional dichotomy: ERα promotes aggression in the ventromedial hypothalamus (VMHvl) while suppressing it in the medial preoptic area (MPOA). Furthermore, social experiences (e.g., victory, isolation) remodel circuit connectivity, revealing profound experience-dependent plasticity. By integrating molecular, circuit, and behavioral insights, we establish a cohesive framework that not only explains the neural underpinnings of aggression but also informs novel strategies for managing its pathological manifestations.
Social play is a rewarding behavior shown across juvenile mammalian species and is important for the development of social competency throughout the lifespan. The neuropeptide oxytocin (OXT) regulates various social beha...Social play is a rewarding behavior shown across juvenile mammalian species and is important for the development of social competency throughout the lifespan. The neuropeptide oxytocin (OXT) regulates various social behaviors and is being used in clinical trials to improve social functioning. However, the role of OXT in juvenile social play is largely unknown. To address this gap, we determined the involvement of hypothalamic OXT-producing neurons in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), PVN projections to the nucleus accumbens (NAc), and OXT signaling within the NAc, in the regulation of social play in juvenile male and female rats. We found that neither chemogenetic stimulation of SON cell bodies nor chemogenetic stimulation of PVN projections to the NAc altered juvenile social play but increased social investigation. However, chemogenetic stimulation of PVN cell bodies as well as acute infusion of OXT into the NAc decreased social play in males without an effect in females. Lastly, social play duration correlated negatively with the proportion of activated NAc neurons, an effect driven by males. Together, these findings suggest that distinct OXT neuronal populations modulate different forms of social behavior and that PVN neurons and OXT signaling in the NAc sex-specifically modulate social play behavior.
Menopause is characterized by the cessation of ovarian hormone production. During postmenopause, cisgender women face increased risks of obesity, cognitive decline, and mood disorder. Mood disorders are associated with e...Menopause is characterized by the cessation of ovarian hormone production. During postmenopause, cisgender women face increased risks of obesity, cognitive decline, and mood disorder. Mood disorders are associated with exposure to chronic stress. We investigated the combined effects of a high-fat diet (HFD) and chronic stress exposure in a mouse model of menopause using 4-vinylcyclohexene diepoxide (VCD), a selective ovotoxicant that gradually depletes ovarian follicles and hormones. Starting at 6 months, 82 female WT C57BL/6 J mice received sesame oil or VCD (130 mg/kg i.p.) 5 days per week for 3 weeks. One month after injection, mice were fed either low-fat diet (LFD) or HFD for 8 weeks followed by 6 weeks of chronic variable mild stress (CVMS). Post-CVMS, mice were either processed for gene expression of the anterodorsal bed nucleus of the stria terminalis (adBNST) or behavior tests to assess cognitive and anxiety-related behaviors. Plasma samples were collected to analyze metabolic hormones and corticosterone levels. VCD-treated HFD-fed mice had higher fat and body mass, and elevated fasting glucose levels compared to controls and more pronounced avoidance behaviors and cognitive impairments. VCD-treated LFD-fed mice exhibited less exploration of novel objects and open spaces compared to sesame oil and HFD counterparts. VCD elevated corticosterone levels on LFD and increased BNST Adcyap1 (PACAP) gene expression on HFD. These findings highlight cognitive repercussions of estrogen deficiency and suggest a potential protective effect of a HFD against some of the adverse outcomes associated with menopause. Our study emphasizes the importance of considering dietary and hormonal interactions in the development of therapeutic strategies.
Pubertal development is regulated by hypothalamic neuroendocrine signaling and is sensitive to interactions between stress- and reproductive-related pathways. In particular, corticotropin-releasing hormone (CRH) signalin...Pubertal development is regulated by hypothalamic neuroendocrine signaling and is sensitive to interactions between stress- and reproductive-related pathways. In particular, corticotropin-releasing hormone (CRH) signaling via corticotropin-releasing hormone receptor 1 (CRHR1) represents a key point of crosstalk between stress and pubertal maturation. Early-life adversity, such as the maternal separation (MS) model in rodents, has been shown to increase CRH expression and therefore has the potential to dysregulate CRHR1 signaling. We previously reported that MS-exposed female rats display early pubertal onset, with heightened anxiety-like behavior that was correlated with pubertal timing. The current study examined whether CRHR1 dysregulation mediates the effects of MS on both pubertal timing and anxiety-like behavior, as assessed by the acoustic startle response (ASR), in female rats. CRHR1 signaling was pharmacologically manipulated using the CRHR1 antagonist antalarmin during MS exposure. Pubertal development and ASR were assessed, as well as pre-pubertal hypothalamic CRHR1 expression. Protein quantification of pre-pubertal hypothalamic cell membrane and cytoplasmic fractions revealed that MS increases CRHR1 internalization in the arcuate nucleus and in the anterior hypothalamus following MS. As expected, MS significantly advanced pubertal timing; however, accelerated puberty was normalized by treatment with antalarmin during MS. Treatment with a high dose of antalarmin, however, delayed puberty in both MS and control animals. MS also increased ASR in adolescent females, which was prevented by antalarmin treatment during MS. Additionally, antalarmin decreased cFos activity in the basolateral amygdala (BLA) and bed nucleus of stria terminalis (BNST). Together, these findings support a potential model in which altered CRHR1 signaling during negative early environments disrupts HPA-HPG axis crosstalk, triggering early onset of puberty and increased anxiety-like behavior in female rats. Targeting CRHR1 signaling during sensitive developmental windows may provide a therapeutic avenue for mitigating these long-term impacts of early life stress.
Parental care varies across reproductive stages, between sexes, and even within individuals. This flexibility raises a key question: does caregiving correspond to distinct circulating hormone profiles, or does it occur w...Parental care varies across reproductive stages, between sexes, and even within individuals. This flexibility raises a key question: does caregiving correspond to distinct circulating hormone profiles, or does it occur within a shared hormonal background that supports rapid, context-dependent shifts in behavior? We investigated these alternatives in red-winged blackbirds (Agelaius phoeniceus), a species in which females always feed nestlings while males range from no provisioning to high rates of chick care. Using continuous nest video recordings (24-48 h) and a panel of circulating hormones (prolactin and four steroids), we examined how hormone profiles relate to breeding stage, sex, and paternal effort. First, courtship-stage males and nestling-stage males were clearly separated by their hormone profiles, confirming that breeding stage is a major axis of endocrine variation. Second, during the nestling-stage, provisioning females and males differed in hormone profiles and in how hormones related to parental effort, indicating sex-specific hormonal modulation within a shared parental context. Third, provisioning and non-provisioning males overlapped broadly in hormone profiles, and no single hormone reliably predicted whether a male provisioned. Instead, associations with parental effort emerged primarily through interactions among hormonal axes. Together, these results indicate that breeding stage and sex strongly organize circulating hormone profiles and that facultative male care operates within a broadly shared endocrine background rather than through discrete hormonal divergence between caregiving categories.
Adolescence is a developmental period during which rising gonadal hormones drive the maturation of neural circuits underlying adult behaviour. Testosterone acts directly via androgen receptors (AR) or indirectly through...Adolescence is a developmental period during which rising gonadal hormones drive the maturation of neural circuits underlying adult behaviour. Testosterone acts directly via androgen receptors (AR) or indirectly through aromatization to estradiol, yet the role of estradiol signalling in refining sexual behaviour during adolescence in male rats remains unclear. We tested whether inhibiting aromatase with fadrozole (FAD) from postnatal day 38 to 48 (around the time of puberty) affects adult sexual behaviour. To determine whether any deficits in sexual behaviour were secondary to anxiety-like behaviour and/or altered stress responding, anxiety-like behaviour and corticosterone release in response to a stressor also were measured. As adults, FAD males did not differ from control (CTL) rats in anxiety-like behaviour, in corticosterone release in response to stress, nor in testosterone concentrations. Aromatase inhibition impaired sexual performance: FAD males mounted, intromitted, and ejaculated less frequently, though sexual motivation and partner preference were preserved. The groups did not differ in AR densities or immunoreactive cell counts in either the medial amygdala or medial preoptic area. Estrogen receptor alpha (ERα) was reduced in the medial amygdala only. These results suggest that aromatization during adolescence refines circuits underlying male sexual behaviour.
The decline of rat maternal behavior during the postpartum period is a critical transition, yet its underlying mechanisms, particularly the interactive effects of the mother's internal state and offspring characteristics...The decline of rat maternal behavior during the postpartum period is a critical transition, yet its underlying mechanisms, particularly the interactive effects of the mother's internal state and offspring characteristics, remain incompletely understood. Using a 3 × 3 factorial design, we examined maternal behavior in Sprague-Dawley rats across three postpartum stages [postpartum day (PPD) 5/6, PPD 11/12, PPD 17/18] when presented with pups of three postnatal ages [postnatal day (PND) 5/6, PND 11/12, PND 17/18]. Behavioral assessments included a home-cage maternal behavior test, a pup retrieval test on an Elevated Plus Maze (EPM), and a pup versus male preference test. Our results demonstrate a dynamic rebalancing of maternal motivations: as pups aged and dams progressed through later postpartum stages, classic approach-related behaviors (e.g., pup retrieval, licking, crouching/hovering over pups) significantly decreased, while withdrawal-related behaviors (e.g., pup avoidance, self-grooming, and dam's distance from the nest) correspondingly increased. This shift was distinctly modulated: pup characteristics primarily influenced the decline in approach motivation, whereas maternal condition predominantly governed the increase in withdrawal motivation. In the EPM, pup age specifically affected pup retrieval and general activity but not anxiety-like behavior. Late-postpartum dams lost their preferential interest in younger pups in the pup versus male preference test. Furthermore, we validated a set of behavioral indicators (e.g., resting away from pups, dam's distance from the nest) as reliable measures of withdrawal motivation. Collectively, these findings underscore that the decline of maternal behavior arises from a dynamic rebalancing between approach and withdrawal motivational systems, jointly driven by the dam's evolving internal state and the changing stimulus characteristics of the developing pups. Additionally, our work extends the Approach-Withdrawal biphasic motivational framework to the natural decline phase of maternal behavior and provides validated tools for assessing withdrawal motivation.
A rapid increase in autism spectrum disorder (ASD) prevalence, high heritability, and higher incidence in boys suggest a role of gene-environment interactions, likely involving sex hormones in its etiology. Prenatal expo...A rapid increase in autism spectrum disorder (ASD) prevalence, high heritability, and higher incidence in boys suggest a role of gene-environment interactions, likely involving sex hormones in its etiology. Prenatal exposure to high testosterone concentration has been linked to risk of ASD, however, experimental proof in genetically predisposed animals is lacking. Since neonatal development in mice mirrors late prenatal neurodevelopment in humans, we investigated the effects of neonatal testosterone administration on the behavior of female and male Shank3b mice. On postnatal day 1, neonate Shank3b and wild-type pups of both sexes received a single dose of testosterone (1 mg) or vehicle subcutaneously. Behavioral phenotyping of mice was conducted in adolescence and adulthood. ASD-like behavior was unaffected by the combination of neonatal exposure to testosterone, male sex, and Shank3b deficiency in both adolescence and adulthood. In adolescence, testosterone-treated mice showed 32% higher object-avoidance behavior in comparison to control mice. Shank3b mice spent threefold longer time self-grooming, buried half as many marbles, and vertically explored 23% less than wild-type mice. In adulthood, neonatal exposure to testosterone reduced vertical exploration by 34% and locomotor activity by 15%. Shank3b mice self-groomed threefold longer, buried 31% fewer marbles, and spent 37% less time by vertical exploration than wild-type mice. Neonatal exposure to testosterone seems to affect object avoidance and exploration, rather than ASD-like behavior. Early testosterone exposure or its synergistic effects with sex and genetic predisposition on the ASD-like phenotype later in life seem to be limited.
The repeated evolution of parental care is often accompanied by shifts in the neural circuits and hormonal pathways that regulate motivation and aggression. Nonapeptides of the oxytocin/vasopressin family, including argi...The repeated evolution of parental care is often accompanied by shifts in the neural circuits and hormonal pathways that regulate motivation and aggression. Nonapeptides of the oxytocin/vasopressin family, including arginine vasotocin (AVT) in teleost fishes, modulate diverse social behaviors across vertebrates such as courtship, pair bonding, parental care, and territoriality. The mechanism behind conservation of these neuromodulators during behavioral diversification remains unclear. We used a comparative pharmacological approach across six darter species (Percidae: Etheostomatinae) by injecting either AVT, an AVT receptor antagonist (Manning's compound), or a vehicle control (saline), followed by physiological and behavioral monitoring in standardized intruder assays. AVT administration significantly increased respiration rate, quantifiable as opercular beats per minute (OBPM) across species, indicating conserved AVT-responsive physiology. In contrast, AVT-evoked aggression varied sharply among lineages: AVT robustly elevated fin flare displays in caregiving species (Etheostoma podostemone, E. nigrum, E. flabellare, and Nothonotus starnesi) and in one non-care species with intense male-male competition (N. rufilineatus), but had no effect in E. vitreum, which has secondarily lost paternal care and spawns communally. This implies that AVT signaling remains physiologically intact, but its behavioral coupling has been selectively strengthened or lost across evolutionary transitions in parental care. These results identify lineage-specific rewiring of nonapeptide control of aggression and establish a framework for cellular and molecular dissection of AVT receptor expression and circuit remodeling in the vertebrate social brain.
Mustoe A, Greig J, Alvarez A
… +15 more, Hinojosa C, Duran J, Melchor A, Comer E, Naseem Y, Arroyo JP, Huber HF, Layne-Colon D, Lambrou E, Callery J, Giavedoni L, Phillips KA, Rothwell ES, Salmon AB, Ross CN
Social relationships are critical for maintaining physical health and psychological wellbeing. Since nearly 1 in 4 adults aged 65 years or older are socially isolated, there is a strong need to understand how repeated so...Social relationships are critical for maintaining physical health and psychological wellbeing. Since nearly 1 in 4 adults aged 65 years or older are socially isolated, there is a strong need to understand how repeated social stress negatively impacts health outcomes. Using a nonhuman primate model of social aging (i.e., marmosets), we examined whether individuals transitioning into old age ("peri-geri") or individuals who were already geriatric ("very-geri") showed differences in measures of hypothalamic-pituitary axis (HPA) activity, markers of metabolic function, and reunion social behavior in response to repeated social separation challenges (SSC). We found female marmosets, especially peri-geri females, had higher HPA reactivity and better HPA recovery than male marmosets, but this difference diminished in older, very-geri marmosets. HPA activity was correlated with multiple outcomes including locomotive behavior and grooming, changes in blood glucose levels, and neutrophil counts, but not estrogens. Marmosets who approached their partner more and were groomed less during reunions had higher cortisol levels the following day. Interestingly, we found two distinct HPA profiles among our marmosets with half showing strong HPA responses (reactors) and the other half showing little or no HPA response (non-reactors). Non-reactors had less weight gain/more weight loss; elevated levels of calcium, phosphorus, and white blood cells; and received less grooming and social contact time during reunion. Overall, old-aged marmosets who show attenuated HPA responses may have different vulnerabilities to negative health and behavioral outcomes during social stress, and male marmosets appear more likely to present with this HPA non-reactor phenotype earlier in aging.
Nighttime exposure to blue light has been shown to disrupt circadian rhythms, brain function, and cognitive behavior. Previous studies in adult rats show that blue light can alter both cognitive and reproductive function...Nighttime exposure to blue light has been shown to disrupt circadian rhythms, brain function, and cognitive behavior. Previous studies in adult rats show that blue light can alter both cognitive and reproductive function. Given the near ubiquitous use of blue light-emitting electronic devices, an emerging concern is the effects of blue light on the developing adolescent brain. In the present study, adolescent (postnatal day P25-55) male and female Long Evans rats were exposed to blue light for 6 h per night followed by 6 h of darkness. Controls were kept on a standard 12:12 h schedule. In early adulthood (P60), subjects underwent a battery of tests to assess anxiety-like behavior, exploratory behavior and learning/memory. Brain tissue was then collected at P90, and prefrontal cortex sections were analyzed. Adolescent blue light exposure altered pubertal onset in a sex-specific manner, and significantly affected performance in the novel object recognition task in both males and females. Blue light also reduced the thickness of the medial prefrontal cortex, but not the motor cortex, in both sexes. These results suggest that adolescent blue light exposure may alter neurodevelopment, with implications for cognition. Future work is needed to further assess the potential clinical implications of ubiquitous nighttime blue light exposure in adolescents.