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Central to the navigation of an ever-changing environment is the ability to form positive associations with places and conspecifics. The functions of location and social conditioned preferences are often studied independently, limiting our understanding of their interplay. Furthermore, a de-emphasis on natural functions of conditioned preferences has led to neurobiological interpretations separated from ecological context. By adopting a naturalistic and ethological perspective, we uncover complexities underlying the expression of conditioned preferences. Development of conditioned preferences is a combination of motivation, reward, associative learning, and context, including for social and spatial environments. Both social- and location-dependent reward-responsive behaviors and their conditioning rely on internal state-gating mechanisms that include neuroendocrine and hormone systems such as opioids, dopamine, testosterone, estradiol, and oxytocin. Such reinforced behavior emerges from mechanisms integrating past experience and current social and environmental conditions. Moreover, social context, environmental stimuli, and internal state gate and modulate motivation and learning via associative reward, shaping the conditioning process. We highlight research incorporating these concepts, focusing on the integration of social neuroendocrine mechanisms and behavioral conditioning. We explore three paradigms: 1) conditioned place preference, 2) conditioned social preference, and 3) social conditioned place preference. We highlight nonclassical species to emphasize the naturalistic applications of these conditioned preferences. To fully appreciate the complex integration of spatial and social information, future research must identify neural networks where endocrine systems exert influence on such behaviors. Such research promises to provide valuable insights into conditioned preferences within a broader naturalistic context. • Both location and social environment affect context-dependent behavioral conditioning. • Endocrine signals interact with reward pathways inducing social and place preferences. • Internal state-gating of conditioning affected by complex stimuli of past and present • Ethologically-relevant conditioning in lab and field highlights natural complexity. • Future studies: endocrine orchestration of preference via multiple brain networks [ABSTRACT FROM AUTHOR]

The neuropeptides arginine vasopressin (AVP) and oxytocin (OXT) are key regulators of social behaviour across vertebrates. However, much of our understanding of how these neuropeptide systems interact with social behaviour is centred around laboratory studies which fail to capture the social and physiological challenges of living in the wild. To evaluate relationships between these neuropeptide systems and social behaviour in the wild, we studied social groups of the cichlid fish Neolamprologus pulcher in Lake Tanganyika, Africa. We first used SCUBA to observe the behaviour of focal group members and then measured transcript abundance of key components of the AVP and OXT systems across different brain regions. While AVP is often associated with male-typical behaviours, we found that dominant females had higher expression of avp and its receptor (avpr1a2) in the preoptic area of the brain compared to either dominant males or subordinates of either sex. Dominant females also generally had the highest levels of leucyl-cystinyl aminopeptidase (lnpep)—which inactivates AVP and OXT—throughout the brain, potentially indicating greater overall activity (i.e. , production, release, and turnover) of the AVP system in dominant females. Expression of OXT and its receptors did not differ across social ranks. However, dominant males that visited the brood chamber more often had lower preoptic expression of OXT receptor a (oxtra) suggesting a negative relationship between OXT signalling and parental care in males of this species. Overall, these results advance our understanding of the relationships between complex social behaviours and neuroendocrine systems under natural settings. • Vasopressin and oxytocin relate to social factors in a wild group-living fish. • Dominant females had higher expression of vasopressin and its receptor. • Nonapeptide inactivating enzyme levels were also higher in dominant females. • Dominant males with fewer oxytocin receptors visited the brood chamber more. [ABSTRACT FROM AUTHOR]

When living in urban habitats, 'urban adapter' species often show greater aggression toward conspecifics, yet we do not understand the mechanisms underlying this behavioral shift. The neuroendocrine system regulates socio-sexual behaviors including aggression and thus could mediate behavioral responses to urbanization. Indeed, urban male song sparrows (Melospiza melodia), which are more territorially aggressive, also have greater abundance of the neuropeptide arginine vasotocin (AVT) in nodes of the brain social behavior network. Higher abundance of AVT could reflect long-term synthesis that underlies baseline territoriality or short-term changes that regulate aggression in response to social challenge. To begin to resolve the timeframe over which the AVT system contributes to habitat differences in aggression we used immediate early gene co-expression as a measure of the activation of AVT neurons. We compared Fos induction in AVT-immunoreactive neurons of the bed nucleus of the stria terminalis (BSTm) and paraventricular nucleus of the hypothalamus (PVN) between urban and rural male song sparrows in response to a short (< 5 min.) or long (> 30 min.) song playback to simulate territorial intrusion by another male. We found that urban males had a higher proportion of Fos-positive AVT neurons in both brain regions compared to rural males, regardless of the duration of song playback. Our results suggest that AVT neurons remain activated in urban males, independently of the duration of social challenge. These findings that Fos induction in AVT neurons differs between rural and urban male song sparrows further implicate this system in regulating behavioral responses to urbanization. • 'Urban adapter' species are often more aggressive when in urban habitats. • Circulating hormones don't reliably explain urban aggression but neuropeptides may. • More aggressive urban sparrows had a greater proportion of activated AVT neurons. • The AVT system could contribute to elevated aggression in urban male song sparrows. [ABSTRACT FROM AUTHOR]

A contribution to SBN/ICN special issue. Endocrine-disrupting chemicals (EDCs) are pervasive in the environment. They are found in plastics and plasticizers (bisphenol A (BPA) and phthalates), in industrial chemicals such as polychlorinated biphenyls (PCBs), and include some pesticides and fungicides such as vinclozolin. These chemicals act on hormone receptors and their downstream signaling pathways, and can interfere with hormone synthesis, metabolism, and actions. Because the developing brain is particularly sensitive to endogenous hormones, disruptions by EDCs can change neural circuits that form during periods of brain organization. Here, we review the evidence that EDCs affect developing hypothalamic neuroendocrine systems, and change behavioral outcomes in juvenile, adolescent, and adult life in exposed individuals, and even in their descendants. Our focus is on social, communicative and sociosexual behaviors, as how an individual behaves with a same- or opposite-sex conspecific determines that individual's ability to exist in a community, be selected as a mate, and reproduce successfully. • Bisphenol A, PCBs, phthalates and vinclozolin are endocrine-disrupting chemicals (EDCs). • EDC exposures change hypothalamic development and organization. • Social and sociosexual behaviors are perturbed by developmental EDC exposures. • There are transgenerational effects of EDCs on social behavior. [ABSTRACT FROM AUTHOR]

Abstract Magnesium (Mg), is not only a modulator of the glutamatergic NMDA receptors' affinity, it also prevents HPA axis hyperactivity, thus possibly being implicated in neurobiological features of mood disorders. Further uncovering of molecular mechanisms underlying magnesium's proposed effects is needed due to the recent shift in research of treatment resistant depression (TRD) towards glutamatergic pathways. Here, we applied Mg via drinking water for 28 days (50 mg/kg/day), in ACTH-treated rats, an established animal model of depression resistant to tricyclic antidepressants. Using this model in male rats we measured (1) changes in hippocampal neurogenesis and behavioral alterations, (2) adrenal hormones response to acute stress challenge and (3) levels of biometals involved in regulation of monoamines turnover in rat prefrontal cortex. Our results support beneficial behavioral impact of Mg in TRD model together with increased hippocampal neurogenesis and BDNF expression. Furthermore, Mg prevented ACTH-induced disruption in HPA axis function, by normalizing the levels of plasma ACTH, corticosterone and interleukin-6, and by increasing the peripheral release of adrenaline, noradrenaline and serotonin after the acute stress challenge. Finally, the influence on copper/zinc ratio suggested probable magnesium's involvement in monoamine turnover in PFC. Our findings provide further insights into the possible pathways implicated in the behavioral modulation effects of Mg, as well as its central and peripheral effects in ACTH-induced TRD model. Thus, further investigation of molecular signaling related to the glutamatergic transmission and role of Mg, could reveal prospects to novel treatment strategies that could be of particular importance for patients suffering from TRD. Highlights • In ACTH model of treatment-resistant depression Mg alleviates behavioral changes. • HPA axis hyperactivity induced by ACTH was attenuated in Mg-administered rats. • Study suggests involvement of Mg in central and peripheral turnover of monoamines. • In ACTH model of treatment-resistant depression Mg increases neurodevelopment. [ABSTRACT FROM AUTHOR]

Fathering behavior is critical for offspring survival in many species across diverse taxa, but our understanding of the neuroendocrine mechanisms regulating paternal care is limited in part because of the few primarily paternal species among the common animal models. However, many teleosts display primarily paternal care, and among the teleosts, anemonefish species are particularly well suited for isolating molecular mechanisms of fathering as they perform parental care in isolation of many other typically competing behaviors such as territorial defense and nest building. The goal of this study was to determine the extent to which whole brain gene expression levels of isotocin receptors, arginine vasotocin receptors, and aromatase as well as circulating levels of the bioactive sex steroid hormones estradiol (E2) and 11-ketotestosterone (11KT) vary in association with parenting behavior in Amphiprion ocellaris . Brain aromatase and IT receptor gene expression were higher in both males and females that were parenting versus not. IT receptor expression was overall higher in males than females, which we interpret is a reflection of the greater parental effort that males display. Aromatase was overall higher in females than males, which we conclude is related to the higher circulating E2, which crosses into the brain and increases aromatase transcription. Results suggest both aromatase and IT receptors are dynamically upregulated in the brains of A. ocellaris males and females to support high levels of parental effort. [ABSTRACT FROM AUTHOR]

Laboratory stress tasks such as the Trier Social Stress Test (TSST) have provided a key piece to the puzzle for how psychosocial stress impacts the hypothalamic-pituitary-adrenal axis, other stress-responsive biomarkers, and ultimately wellbeing. These tasks are thought to work through biopsychosocial processes, specifically social evaluative threat and the uncontrollability heighten situational demands. The present study integrated an experimental modification to the design of the TSST to probe whether additional social evaluative threat, via negative verbal feedback about speech performance, can further alter stress reactivity in 63 men and women. This TSST study confirmed previous findings related to stress reactivity and stress recovery but extended this literature in several ways. First, we showed that additional social evaluative threat components, mid-task following the speech portion of the TSST, were still capable of enhancing the psychosocial stressor. Second, we considered stress-reactive hormones beyond cortisol to include dehydroepiandrosterone (DHEA) and testosterone, and found these hormones were also stress-responsive, and their release was coupled with one another. Third, we explored whether gain- and loss-framing incentive instructions, meant to influence performance motivation by enhancing the personal relevance of task performance, impacted hormonal reactivity. Results showed that each hormone was stress reactive and further had different responses to the modified TSST compared to the original TSST. Beyond the utility of showing how the TSST can be modified with heightened social evaluative threat and incentive-framing instructions, this study informs about how these three stress-responsive hormones have differential responses to the demands of a challenge and a stressor. [ABSTRACT FROM AUTHOR]

A contribution to a special issue on Hormones and Human Competition.The ease of measuring steroids in saliva has led to an increase in investigating their role in competition and aggression in laboratory settings and using behavioral measures of aggression. We review here the Point-Subtraction-Aggression-Paradigm (PSAP) as a measure of costly aggression and we compare and contrast the PSAP to other aggression measures. We describe our use of the PSAP, highlighting how it can be modified to investigate a broad array of experimental questions. We review studies that have investigated neuroendocrine function and the PSAP, and we conclude that across studies the relationship between fluctuations in testosterone and PSAP aggression scores are directionally positive, and are likely specific to men. Investigations of other neuroendocrine measures and the PSAP are fewer, limiting conclusions that can be drawn for other hormones. We provide two versions of the PSAP that can be used with E-PRIME® software for researchers interested in this measure for their laboratories. [ABSTRACT FROM AUTHOR]

Primates maintain a variety of social relationships and these can have fitness consequences. Research has established that different types of social relationships are unpinned by different or interacting hormonal systems, for example, the neuropeptide oxytocin influences social bonding, the steroid hormone testosterone influences dominance relationships, and paternal care is characterized by high oxytocin and low testosterone. Although the oxytocinergic system influences social bonding, it can support different types of social bonds in different species, whether pair bonds, parent-offspring bonds or friendships. It seems that selection processes shape social and mating systems and their interactions with neuroendocrine pathways. Within species, there are individual differences in the development of the neuroendocrine system: the social environment individuals are exposed to during ontogeny alters their neuroendocrine and socio-cognitive development, and later, their social interactions as adults. Within individuals, neuroendocrine systems can also have short-term effects, impacting on social interactions, such as those during hunting, intergroup encounters or food sharing, or the likelihood of cooperating, winning or losing. To understand these highly dynamic processes, extending research beyond animals in laboratory settings to wild animals living within their natural social and ecological setting may bring insights that are otherwise unreachable. Field endocrinology with neuropeptides is still emerging. We review the current status of this research, informed by laboratory studies, and identify questions particularly suited to future field studies. We focus on primate social relationships, specifically social bonds (mother-offspring, father-offspring, cooperative breeders, pair bonds and adult platonic friendships), dominance, cooperation and in-group/out-group relationships, and examine evidence with respect to the ‘tend and defend’ hypothesis. [ABSTRACT FROM AUTHOR]

The immune system plays an important role in enhancing an individual's ability to survive in a world inhabited by pathogens and parasites. The innate immune system is regulated by processes encoded in an individual's genome, providing an avenue for selection to act on this system, as well as the phenotypic relationships generated between this system and other traits of interest. While relationships between innate immunity and endocrine traits (e.g. testosterone) have been reported often in the literature, these relationships are complex and may differ under varying environmental conditions. To better understand the relative contribution of innate immunity (or an endocrine or behavioral trait) to a phenotypic correlation with another trait, an estimation of the underlying heritable genetic variation of the trait of interest is needed. An upper level estimate of the heritability of such traits can be obtained from calculating its repeatability. We conducted a literature review to determine how often repeated samples of measures of innate immune function were conducted and repeatability estimates obtained. This review revealed a very limited number of repeatability estimates, with a large range (0.0–0.9); estimates were exclusively from livestock that have undergone strong artificial selection. This observation of the present literature suggests more work is needed in non-domesticated and free-living animals to begin to understand the underlying genetic contribution of innate immune function to phenotypic correlations of interest (e.g. testosterone and immunity) to behavioral ecologists, evolutionary physiologists and ecoimmunologists. [ABSTRACT FROM AUTHOR]

The comparison between immune and neuroendocrine systems in vertebrates and invertebrates suggest an ancient origin and a high degree of conservation for the mechanisms underlying the integration between immune and stress responses. This suggests that in both vertebrates and invertebrates the stress response involves the integrated network of soluble mediators ( e.g. , neurotransmitters, hormones and cytokines) and cell functions ( e.g. , chemotaxis and phagocytosis), that interact with a common objective, i.e. , the maintenance of body homeostasis. During evolution, several changes observed in the stress response of more complex taxa could be the result of new roles of ancestral molecules, such as ancient immune mediators may have been recruited as neurotransmitters and hormones, or vice versa . We review older and recent evidence suggesting that immune and neuro-endocrine functions during the stress response were deeply intertwined already at the dawn of multicellular organisms. These observations found relevant reflections in the demonstration that immune cells can transdifferentiate in olfactory neurons in crayfish and the recently re-proposed neural transdifferentiation in humans. [ABSTRACT FROM AUTHOR]

Clinical and experimental evidence shows that estrogens affect immunity in mammals. Less is known about this interaction in the evolutionary older, non-mammalian, vertebrates. Fish form an excellent model to identify evolutionary conserved neuroendocrine-immune interactions: i) they are the earliest vertebrates with fully developed innate and adaptive immunity, ii) immune and endocrine parameters vary with season, and iii) physiology is constantly disrupted by increasing contamination of the aquatic environment. Neuro-immuno-endocrine interactions enable adaption to changing internal and external environment and are based on shared signaling molecules and receptors. The presence of specific estrogen receptors on/in fish leukocytes, implies direct estrogen-mediated immunoregulation. Fish leukocytes most probably are also capable to produce estrogens as they express the cyp19a and cyp19b – genes, encoding aromatase cytochrome P450, the enzyme critical for conversion of C19 steroids to estrogens. Immunoregulatory actions of estrogens, vary among animal species, and also with dose, target cell type, or physiological condition (e.g., infected/non-infected, reproductive status). They moreover are multifaceted. Interestingly, season-dependent changes in immune status correlate with changes in the levels of circulating sex hormones. Whereas E2 circulating in the bloodstream is perhaps the most likely candidate to be the physiological mediator of systemic immune-reproductive trade-offs, leukocyte-derived hormones are hypothesized to be mainly involved in local tuning of the immune response. Contamination of the aquatic environment with estrogenic EDCs may violate the delicate and precise allostatic interactions between the endogenous estrogen system and the immune system. This has negative effects on fish health, but will also affect the physiology of its consumers. [ABSTRACT FROM AUTHOR]

Multidirectional interactions among the immune, endocrine, and nervous systems have been demonstrated in humans and non-human animal models for many decades by the biomedical community, but ecological and evolutionary perspectives are lacking. Neuroendocrine-immune interactions can be conceptualized using a series of feedback loops, which culminate into distinct neuroendocrine-immune phenotypes. Behavior can exert profound influences on these phenotypes, which can in turn reciprocally modulate behavior. For example, the behavioral aspects of reproduction, including courtship, aggression, mate selection and parental behaviors can impinge upon neuroendocrine-immune interactions. One classic example is the immunocompetence handicap hypothesis (ICHH), which proposes that steroid hormones act as mediators of traits important for female choice while suppressing the immune system. Reciprocally, neuroendocrine-immune pathways can promote the development of altered behavioral states, such as sickness behavior. Understanding the energetic signals that mediate neuroendocrine-immune crosstalk is an active area of research. Although the field of psychoneuroimmunology (PNI) has begun to explore this crosstalk from a biomedical standpoint, the neuroendocrine-immune-behavior nexus has been relatively underappreciated in comparative species. The field of ecoimmunology, while traditionally emphasizing the study of non-model systems from an ecological evolutionary perspective, often under natural conditions, has focused less on the physiological mechanisms underlying behavioral responses. This review summarizes neuroendocrine-immune interactions using a comparative framework to understand the ecological and evolutionary forces that shape these complex physiological interactions. [ABSTRACT FROM AUTHOR]

The regulation of seasonality has been an area of interest for decades, yet global climate change has created extra urgency in the quest to understand how sensory circuits and neuroendocrine control systems interact to generate flexibility in biological timekeeping. The capacity of temperature to alter endogenous or photoperiod-regulated neuroendocrine mechanisms driving seasonality, either as a direct cue or through temperature-dependent effects on energy and metabolism, is at the heart of this phenological flexibility. However, until relatively recently, little research had been done on the integration of temperature information in canonical seasonal neuroendocrine pathways, particularly in vertebrates. We review recent advances from research in vertebrates that deepens our understanding of how temperature cues are perceived and integrated into seasonal hypothalamic thyroid hormone (TH) signaling, which is a critical regulator of downstream seasonal phenotypic changes such as those regulated by the BPG (brain-pituitary-gonadal) axis. Temperature perception occurs through cutaneous transient receptor potential (TRP) neurons, though sensitivity of these neurons varies markedly across taxa. Although photoperiod is the dominant cue used to trigger seasonal physiology or entrain circannual clocks, across birds, mammals, fish, reptiles and amphibians, seasonality appears to be temperature sensitive and in at least some cases this appears to be related to phylogenetically conserved TH signaling in the hypothalamus. Nevertheless, the exact mechanisms through which temperature modulates seasonal neuroendocrine pathways remains poorly understood. • Seasonal neuroendocrine pathways are sensitive to temperature. • Taxa differ in temperature sensitivity. • Differences may arise during temperature perception, integration, and transduction. • Important targets for research are TRPs and seasonal thyroid hormone signaling. [ABSTRACT FROM AUTHOR]

Studies of social stress in adult mice have revealed two distinct defeat-responsive behavioral phenotypes; “susceptible” and “resistant,” characterized by social avoidance and social interaction, respectively. Typically, these phenotypes are observed at least 1 day after the last defeat in adults, but may extend up to 30 days later. The current study examined the impact of peripubertal social defeat on immediate (1 day) and adult (30 day) social stress phenotypes and neuroendocrine function in male C57BL/6 mice. Initially, peripubertal (P32) mice were resistant to social defeat. When the same mice were tested for social interaction again as adults (P62), two phenotypes emerged; a group of mice were characterized as susceptible evidenced by significantly lower social interaction, whereas the remaining mice exhibited normal social interaction, characteristic of resistance. A repeated analysis of corticosterone revealed that the adult (P62) resistant mice had elevated corticosterone following the social interaction test as juveniles. This was when all mice, regardless of adult phenotype, displayed equivalent levels of social interaction. Peripubertal corticosterone was positively correlated with adult social interaction levels in defeated mice, suggesting early life stress responsiveness impacts adult social behavior. In addition, adult corticotropin-releasing factor (CRF) mRNA in the paraventricular nucleus of the hypothalamus (PVN) was elevated in all defeated mice, but there were no differences in CRF mRNA expression between the phenotypes. Thus, there is a delayed appearance of social stress-responsive phenotypes suggesting that early life stress exposure, combined with the resultant physiological responses, may interact with pubertal development to influence adult social behavior. [ABSTRACT FROM AUTHOR]

This article is part of a Special Issue "Parental Care". Although paternal care is generally rare among vertebrates, care of eggs and young by male birds is extremely common and may take on a variety of forms across species. Thus, birds provide ample opportunities for investigating both the evolution of and the proximate mechanisms underpinning diverse aspects of fathering behavior. However, significant gaps remain in our understanding of the endocrine and neuroendocrine influences on paternal care in this vertebrate group. In this review, I focus on proximate mechanisms of paternal care in birds. I place an emphasis on specific hormones that vary predictably and/or unpredictably during the parental phase in both captive and wild birds: prolactin and progesterone are generally assumed to enhance paternal care, whereas testosterone and corticosterone are commonly—though not always correctly—assumed to inhibit paternal care. In addition, because endocrine secretions are not the sole mechanistic influence on paternal behavior, I also explore potential roles for certain neuropeptide systems (specifically the oxytocin–vasopressin nonapeptides and gonadotropin inhibitory hormone) and social and experiential factors in influencing paternal behavior in birds. Ultimately, mechanistic control of fathering behavior in birds is complex, and I suggest specific avenues for future research with the goal of narrowing gaps in our understanding of this complexity. Such avenues include (1) experimental studies that carefully consider not only endocrine and neuroendocrine mechanisms of paternal behavior, but also the ecology, phylogenetic history, and social context of focal species; (2) investigations that focus on individual variation in both hormonal and behavioral responses during the parental phase; (3) studies that investigate mechanisms of maternal and paternal care independently, rather than assuming that the mechanistic foundations of care are similar between the sexes; (4) expansion of work on interactions of the neuroendocrine system and fathering behavior to a wider array of paternal behaviors and taxa (e.g., currently, studies of the interactions of testosterone and paternal care largely focus on songbirds, whereas studies of the interactions of corticosterone, prolactin, and paternal care in times of stress focus primarily on seabirds); and (5) more deliberate study of exceptions to commonly held assumptions about hormone–paternal behavior interactions (such as the prevailing assumptions that elevations in androgens and glucocorticoids are universally disruptive to paternal care). Ultimately, investigations that take an intentionally integrative approach to understanding the social, evolutionary, and physiological influences on fathering behavior will make great strides toward refining our understanding of the complex nature by which paternal behavior in birds is regulated. [ABSTRACT FROM AUTHOR]

This article is part of a Special Issue “Parental Care”. Paternal care, though rare among mammals, is routinely displayed by several species of rodents. Here we review the neuroanatomical and hormonal bases of paternal behavior, as well as the behavioral and neuroendocrine consequences of paternal behavior for offspring. Fathering behavior is subserved by many of the same neural substrates which are also involved in maternal behavior (for example, the medial preoptic area of the hypothalamus). While gonadal hormones such as testosterone, estrogen, and progesterone, as well as hypothalamic neuropeptides such as oxytocin and vasopressin, and the pituitary hormone prolactin, are implicated in the activation of paternal behavior, there are significant gaps in our knowledge of their actions, as well as pronounced differences between species. Removal of the father in biparental species has long-lasting effects on behavior, as well as on these same neuroendocrine systems, in offspring. Finally, individual differences in paternal behavior can have similarly long-lasting, if more subtle, effects on offspring behavior. Future studies should examine similar outcome measures in multiple species, including both biparental species and closely related uniparental species. Careful phylogenetic analyses of the neuroendocrine systems presumably important to male parenting, as well as their patterns of gene expression, will also be important in establishing the next generation of hypotheses regarding the regulation of male parenting behavior. [ABSTRACT FROM AUTHOR]

This article is part of a Special Issue “SBN 2014”. Maternal obesity, metabolic state, and diet during gestation have profound effects on offspring development. The prevalence of neurodevelopmental and mental health disorders has risen rapidly in the last several decades in parallel with the rise in obesity rates. Evidence from epidemiological studies indicates that maternal obesity and metabolic complications increase the risk of offspring developing behavioral disorders such as attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and schizophrenia. Animal models show that a maternal diet high in fat similarly disrupts behavioral programming of offspring, with animals showing social impairments, increased anxiety and depressive behaviors, reduced cognitive development, and hyperactivity. Maternal obesity, metabolic conditions, and high fat diet consumption increase maternal leptin, insulin, glucose, triglycerides, and inflammatory cytokines. This leads to increased risk of placental dysfunction, and altered fetal neuroendocrine development. Changes in brain development that likely contribute to the increased risk of behavioral and mental health disorders include increased inflammation in the brain, as well as alterations in the serotonergic system, dopaminergic system and hypothalamic–pituitary–adrenal (HPA) axis. [ABSTRACT FROM AUTHOR]

Most animals in the temperate zone exhibit robust seasonal rhythms in neuroendocrine, physiological and behavioral processes. The integration of predictive and supplementary environmental cues (e.g., nutrients) involves a series of discrete, and interconnected brain regions that span hypothalamic, thalamic, mesencephalic, and limbic regions. Species-specific adaptive changes in these neuroendocrine structures and cellular plasticity have likely evolved to support seasonal life-history transitions. Despite significant advances in our understanding of ecological responses to predictive and supplementary environmental cues, there remains a paucity of literature on how these diverse cues impact the underlying neural and cellular substrates. To date, most scientific approach has focused on neuroendocrine responses to annual changes in daylength, referred to as photoperiod, due to the robust physiological changes to light manipulations in laboratory settings. In this review, we highlight the relatively few animal models that have been effectively used to investigate how predictive day lengths, and supplementary cues are integrated across hypothalamic nuclei, and discuss key findings of how seasonal rhythms in physiology are governed by adaptive neuroendocrine changes. We discuss how specific brain regions integrate environmental cues to form a complex multiunit or 'modular' system that has evolved to optimize the timing of seasonal physiology. Overall, the review aims to highlight the existence of a modular network of neural regions that independently contribute to timing seasonal physiology. This paper proposes that a multi-modular neuroendocrine system has evolved in which independent neural 'units' operate to support species-specific seasonal rhythms. • Predictive and supplementary external cues fine tune timing of seasonal physiology. • Seasonal rhythms are driven by endogenous programmed changes in physiology. • Discrete neural and cellular processes integrate different environmental cues. • A multi-modal neuroendocrine system for the control of seasonal rhythms is proposed. • Modular perspective shows natural selection acts independently on neural substrates. [ABSTRACT FROM AUTHOR]

Position in a dominance hierarchy profoundly impacts group members' survival, health, and reproductive success. Thus, understanding the mechanisms that regulate or are associated with an individuals' social position is important. Across taxa, various endocrine and neuroendocrine signaling systems are implicated in the control of social rank. Cichlid fishes, with their often-limited resources of food, shelter, and mates that leads to competition, have provided important insights on the proximate and ultimate mechanisms related to establishment and maintenance of dominance hierarchies. Here we review the existing information on the relationships between endocrine (e.g., circulating hormones, gonadal and other tissue measures) and neuroendocrine (e.g., central neuropeptides, biogenic amines, steroids) systems and dominant and subordinate social rank in male cichlids. Much of the current literature is focused on only a few representative cichlids, particularly the African Astatotilapia burtoni , and several other African and Neotropical species. Many hormonal regulators show distinct differences at multiple biological levels between dominant and subordinate males, but generalizations are complicated by variations in experimental paradigms, methodological approaches, and in the reproductive and parental care strategies of the study species. Future studies that capitalize on the diversity of hierarchical structures among cichlids should provide insights towards better understanding the endocrine and neuroendocrine mechanisms contributing to social rank. Further, examination of this topic in cichlids will help reveal the selective pressures driving the evolution of endocrine-related phenotypic traits that may facilitate an individual's ability to acquire and maintain a specific social rank to improve survival and reproductive success. • Endocrine/neuroendocrine systems related to male cichlid social rank are reviewed. • Dominant and subordinate male cichlids show distinct endocrine profiles. • Many endocrine/neuroendocrine systems interact, making generalizations difficult. • Cichlids are excellent models for future work on hormones and dominance hierarchies. [ABSTRACT FROM AUTHOR]

Abstract: One of the fundamental principles of the life-history theory is that parents need to balance their resources between current and future offspring. Deserting the dependent young is a radical life-history decision that saves resources for future reproduction but that may cause the current brood to fail. Despite the importance of desertion for reproductive success, and thus fitness, the neuroendocrine mechanisms of brood desertion are largely unknown. We investigated two candidate hormones that may influence brood desertion in the Kentish plover Charadrius alexandrinus: prolactin (‘parental hormone’) and corticosterone (‘stress hormone’). Kentish plovers exhibit an unusually diverse mating and parental care system: brood desertion occurs naturally since either parent (the male or the female) may desert the brood after the chicks hatch and mate with a new partner shortly after. We measured the hormone levels of parents at hatching using the standard capture and restraint protocol. We subsequently followed the broods to determine whether a parent deserted the chicks. We found no evidence that either baseline or stress-induced prolactin levels of male or female parents predicted brood desertion. Although stress-induced corticosterone levels were generally higher in females compared with males, individual corticosterone levels did not explain the probability of brood desertion. We suggest that, in this species, low prolactin levels do not trigger brood desertion. In general, we propose that the prolactin stress response does not reflect overall parental investment in a species where different parts of the breeding cycle are characterized by contrasting individual investment strategies. [Copyright &y& Elsevier]

Nearly all organisms alter physiological and behavioral activities across the twenty-four-hour day. Endogenous timekeeping mechanisms, which are responsive to environmental and internal cues, allow organisms to anticipate predictable environmental changes and time their daily activities. Among-individual variation in the chronotype, or phenotypic output of these timekeeping mechanisms (i.e. timing of daily behaviors), is often observed in organisms studied under naturalistic environmental conditions. The neuroendocrine system, including sex steroids, has been implicated in the regulation and modulation of endogenous clocks and their behavioral outputs. Numerous studies have found clear evidence that sex steroids modulate circadian and daily timing of activities in captive animals under controlled conditions. However, little is known about how sex steroids influence daily behavioral rhythms in wild organisms or what, if any, implication this may have for survival and reproductive fitness. Here we review the evidence that sex steroids modulate daily timing in vertebrates under controlled conditions. We then discuss how this relationship may be relevant for the reproductive success and fitness of wild organisms and discuss the limited evidence that sex steroids modulate circadian rhythms in wild organisms. • Individual variation in timing of daily behaviors is observed in wild organisms. • Sex steroids modulate circadian and daily timing of activities in captive animals. • Behavioral rhythms in wild organisms often differ from those in captivity. • Little is known about how sex steroids impact daily behavioral rhythms in the wild. [ABSTRACT FROM AUTHOR]

In this paper I discuss how the challenge hypothesis (Wingfield et al., 1990) influenced the development of ideas about animal personality, and describe particularly promising areas for future study at the intersection of these two topics. I argue that the challenge hypothesis influenced the study of animal personality in at least three specific ways. First, the challenge hypothesis drew attention to the ways in which the environment experienced by an organism – including the social environment – can influence biological processes internal to the organism, e.g. changes to physiology, gene expression, neuroendocrine state and epigenetic modifications. That is, the challenge hypothesis illustrated the bidirectional, dynamic relationship between hormones and (social) environments, thereby helping us to understand how behavioral variation among individuals can emerge over time. Because the paper was inspired by data collected on free living animals in natural populations, it drew behavioral ecologists' attention to this phenomenon. Second, the challenge hypothesis highlighted what became a paradigmatic example of a hormonal mechanism for a behavioral spillover, i.e. testosterone's pleiotropic effects on both territorial aggression and parental care causes aggression to "spillover" to influence parenting behavior, thereby limiting behavioral plasticity. Third, the challenge hypothesis contributed to what is now a cottage industry examining individual differences in hormone titres and their relationship with behavioral variation. I argue that one particularly promising future research direction in this area is to consider the active role of behavior and behavioral types in eliciting social interactions, including territorial challenges. • The challenge hypothesis influenced the study of animal personality. • The challenge hypothesis drew attention to the ways the social environment influences the neuroendocrine system. • The challenge hypothesis provided what became a paradigmatic example of limited plasticity. • The challenge hypothesis stimulated researchers to quantify individual variation in circulating hormone titres. [ABSTRACT FROM AUTHOR]

Consistent between-individual differences in behaviour have been documented across the animal kingdom. Such variation between individuals has been shown to be the basis for selection and to act as a pacemaker for evolutionary change. Recently, equivocal evidence suggests that such consistent between-individual variation is also present in hormones. This observation has sparked interest in understanding the mechanisms shaping individual differences, temporal consistency and heritability of hormonal phenotypes and to understand, if and to what extent hormonal mechanisms are involved in mediating consistent variation in behaviour between individuals. Here, we used zebra finches of the fourth generation of bi-directionally selected lines for three independent behaviours: aggression, exploration and fearlessness. We investigated how these behaviours responded to artificial selection and tested their repeatability. We further tested for repeatability of corticosterone and testosterone across and within lines. Moreover, we are presenting the decomposed variance components for within-individual variance (i.e. flexibility) and between-individual variance (i.e. more or less pronounced differences between individuals) and investigate their contribution to repeatability estimates. Both hormones as well as the exploration and fearlessness but not aggressiveness, were repeatable. However, variance components and hence repeatability differed between lines and were often lower than in unselected control animals, mainly because of a reduction in between-individual variance. Our data show that artificial selection (including active selection and genetic drift) can affect the mean and variance of traits. We stress the importance for understanding how variable a trait is both between and within individuals to assess the selective value of a trait. • Aggression and fearlessness respond to artificial selection, exploration does not. • Corticosterone and testosterone levels are repeatable. • Selection on aggression, fearlessness and exploration do not affect TESTO. • Birds selected for low aggressiveness show higher baseline CORT levels. [ABSTRACT FROM AUTHOR]

The hypothalamic-pituitary-adrenal (HPA) axis is the main neuroendocrine system that controls stress responses, including fear learning. To further understand the correlation between the HPA axis and stress- and fear-related symptoms in humans, the current study investigated the relationship between HPA axis gene polymorphisms and a stress- and fear-related disorder, posttraumatic stress disorder (PTSD). This is the first study that systematically investigates the correlations between HPA axis genes and distinct PTSD symptom clusters. Participants included 1132 Chinese earthquake survivors (772 women and 360 men). PTSD symptoms were measured by the PTSD Checklist for DSM - 5 (PCL-5), and the severity (total symptoms) and symptom clusters were calculated according to the hybrid seven-factor model of DSM - 5 PTSD. We genotyped eight single nucleotide polymorphisms (SNPs) of three HPA axis genes, including FKBP5 , CRHR1 and CRHR2. The main effects of the CRHR2 SNP rs2267715 were associated with PTSD severity (P = 0.0035) and all PTSD symptom clusters except dysphoric arousal (P ranging from 0.0011 to 0.048). In women, a gene–environment interaction (G × E) effect of FKBP5 (rs3800373 × trauma exposure) was correlated with PTSD severity (P = 0.038), externalizing behaviors, anxious arousal and dysphoric arousal symptoms (P ranging from 0.014 to 0.028); the G × E effect of CRHR1 (rs4458044 × trauma exposure) was associated with anxious arousal symptoms (P = 0.016). In men, a gene–gene interaction (G × G) effect of FKBP5 – CRHR1 (rs9470080 × rs4458044) was associated with PTSD severity (P = 0.0091), intrusion, negative affect, externalizing behaviors and anxious arousal (P ranging 0.012–0.049). Our results systematically revealed that the main effects and G × E and G × G effects of some genetic polymorphisms of HPA axis genes are involved in the severity and distinct symptom clusters of PTSD. • Main, G × E and G × G effects, as well as distinct PTSD symptom clusters were focused. • HPA axis gene polymorphisms were involved in distinct symptom clusters of PTSD. • FKBP5 seemed to be a key gene regulating stress response via various manners. [ABSTRACT FROM AUTHOR]

Early-life experiences can shape adult behavior, with consequences for fitness and health, yet fundamental questions remain unanswered about how early-life social experiences are translated into variation in brain and behavior. The African cichlid fish Astatotilapia burtoni , a model system in social neuroscience, is well known for its highly plastic social phenotypes in adulthood. Here, we rear juveniles in either social groups or pairs to investigate the effects of early-life social environments on behavior and neuroendocrine gene expression. We find that both juvenile behavior and neuroendocrine function are sensitive to early-life effects. Behavior robustly co-varies across multiple contexts (open field, social cue investigation, and dominance behavior assays) to form a behavioral syndrome, with pair-reared juveniles towards the end of syndrome that is less active and socially interactive. Pair-reared juveniles also submit more readily as subordinates. In a separate cohort, we measured whole brain expression of stress and sex hormone genes. Expression of glucocorticoid receptor 1a was elevated in group-reared juveniles, supporting a highly-conserved role for the stress axis mediating early-life effects. The effect of rearing environment on androgen receptor α and estrogen receptor α expression was mediated by treatment duration (1 vs. 5 weeks). Finally, expression of corticotropin-releasing factor and glucocorticoid receptor 2 decreased significantly over time. Rearing environment also caused striking differences in gene co-expression, such that expression was tightly integrated in pair-reared juveniles but not group-reared or isolates. Together, this research demonstrates the important developmental origins of behavioral phenotypes and identifies potential behavioral and neuroendocrine mechanisms. • Early-life environments and experiences shape neural and behavioral phenotype. • Rearing environment shapes juvenile behavior along a novel behavioral syndrome. • Pair-reared juveniles are less active and interactive, and more subordinate. • The early environment alters neural stress and sex hormone gene expression. • Early environment shifts glucocorticoid, androgen, and estrogen receptor expression. [ABSTRACT FROM AUTHOR]