Parent-offspring communication is fundamental to reproductive success, yet how ecological variation shapes nestling begging behavior, physiology, and parental provisioning remain understudied in free-living systems. We investigated these relationships in free-living northern house wrens (Troglodytes aedon) breeding across an urbanization gradient differing in food availability. Within each population, we experimentally supplemented half of the nests with mealworms while the remaining nests served as non-supplemented controls to determine whether food availability alters offspring begging behavior, parental provisioning, and baseline corticosterone concentrations. Parent-offspring communication changed markedly with nestling age. At 5-6 days, begging intensity primarily reflected the interaction between parental provisioning and seasonal timing, whereas by 11 days it reflected local food availability and nestling body mass. This developmental shift was accompanied by changes in parental provisioning: as nestlings aged, parents relied increasingly on offspring behavior when allocating food. Nestlings with higher begging scores were more likely to receive food, but successful food acquisition depended primarily on the timing of begging relative to parental feeding decisions rather than on begging duration alone. Food supplementation weakened population differences in parent-offspring communication, indicating that variation in food availability underlies much of the observed behavioral variation. Baseline corticosterone concentrations decreased with increasing food intake only in the population with the lowest food availability. Furthermore, larger nestlings exhibited higher baseline corticosterone concentrations under conditions of high begging intensity and low parental provisioning. In contrast, natural variation in baseline corticosterone did not predict begging behavior, suggesting that baseline corticosterone reflects the energetic and ecological context in which begging occurs rather than acting as its direct driver. Our findings demonstrate that parent-offspring communication is highly context dependent and changes substantially during development, highlighting the importance of considering both offspring behavior and ecological context when studying the evolution of parent-offspring interactions.

The renin-angiotensin system (RAS), traditionally recognized for cardiovascular and renal regulation, has emerged as a critical mechanistic player in neuropsychiatric pathophysiology. The brain possesses its own independent RAS with components located throughout limbic regions, cortical areas, and monoaminergic circuits that are essential for mood, cognition, and behavior. Within this framework, angiotensin II (Ang II), acts primarily through angiotensin II type 1 receptors (AT1Rs), orchestrates pathological cascades including nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-mediated oxidative stress and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-driven neuroinflammation which converge to disrupt synaptic plasticity, impair neurogenesis, compromise blood-brain barrier (BBB) integrity, and dysregulate hypothalamic-pituitary-adrenal axis (HPA) axis- all contributing to major depression, anxiety disorders, schizophrenia, and bipolar disorder. However, the brain also contains protective RAS pathways, including angiotensin II Type 2 receptors (AT2Rs) and the angiotensin-converting enzyme 2/ Angiotensin-(1-7)/ Mas receptor (ACE2/Ang-(1-7)/MasR) axis, which offer neuroprotective effects that counterbalance these damaging processes. Therefore, targeting the RAS may represent a paradigm shift in neuropsychiatric treatment, as medications that modulate this system- including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)- show significant promise by addressing the fundamental molecular mechanisms driving mental illness rather than merely managing symptoms. Ultimately, this approach bridges peripheral physiological dysregulation with central nervous system (CNS) dysfunction, offering a precision medicine strategy that targets the root biological causes of neuropsychiatric disorders and opens new therapeutic avenues for patients who may not respond adequately to conventional treatments.

Exercise promotes cognitive function and stress resilience in both fishes and mammals. In mammals, these effects are linked to reward mechanisms, particularly when exercise is voluntary. Whether exercise engages comparable mechanisms in fishes remains unclear. This is partly due to salmonid research relying almost entirely on forced swimming, which removes the behavioural agency associated with the enhanced effects of voluntary exercise in mammals. We tested whether juvenile Atlantic salmon would choose to swim against a current when a calm zone (i.e. no current) alternative remained available, and whether doing so was associated with changes in stress physiology and monoaminergic signalling. Schools of five fish were tested once, without acclimation, in an arena offering either a body-length-scaled velocity gradient adjoining a calm zone (exercise choice) or calm water only throughout the arena (control). Exercise-choice schools used the flow zone more than controls used the equivalent space, and increasingly so across the trial. Notably, this escalation in the use of the flow zone was confined to the highest velocities. Moreover, exercise-choice schools entered the flow zone less often than controls, yet by the final 20-min interval their longest single bout in the flow took up an average of 96% of the interval. The exercise-choice fish nonetheless continued to use the calm zone throughout, spending 8.8% of tracked time there against 27.6% in controls. Schools with access to flow were also more cohesive, and the fish had, on average, 28% lower plasma cortisol as well as higher dopaminergic and serotonergic signalling in the dorsomedial pallium, a region implicated in affective processing. This experiment demonstrates self-selected exercise in a non-mammalian species, indicating that joint provision of flowing and calm water, enabling agency over swimming duration, warrants further investigation as a welfare intervention in captive salmon.

Phytoestrogens are plant secondary compounds that can bind to estrogen receptors and mimic or modulate endogenous estrogen activity, with potential downstream physiological and behavioral effects. To test whether daily variation in wild estrogenic plant consumption was associated with subsequent variation in fecal steroid hormone concentrations, we sequentially followed six individually recognized Ugandan red colobus monkeys (Piliocolobus tephrosceles) in Kibale National Park, Uganda, over an eight-month study period, collecting 1318 h of behavioral observations and 516 fecal samples. On average, 17.7% of the daily diet consisted of foods with measurable estrogenic activity. Linear mixed-effects models indicated that greater estrogenic plant consumption was associated with lower fecal estradiol concentrations the following day and higher concentrations two and three days later. Cortisol showed no significant relationship with estrogenic plant consumption at any timescale. Variation in fecal estradiol was also associated with time spent moving and feeding but not with sex or time of defecation. These results demonstrate a lagged association between daily phytoestrogen consumption and fecal estradiol excretion patterns at the individual level but do not establish a causal endocrine effect. Longer-term studies incorporating more individuals and reproductive data are needed to determine the biological significance of these associations.

Decision-making circuits are modulated across life stages (e.g. juvenile, adolescent, or adult)-as well as on the shorter timescale of reproductive cycles in females-to meet changing environmental and physiological demands. Ovarian hormone signaling may contribute to this flexibility by regulating neural circuits involved in adaptive decision making. Here, we examined how prepubertal ovariectomy (pOVX) influences adult performance in an odor-guided multiple-choice reversal task. During reversal learning, pOVX females exhibited a distinct pattern of errors compared to sham-operated controls. Reinforcement learning models fit to trial-by-trial behavior showed that the inverse temperature parameter (β) increased during Reversal in sham females, consistent with a shift toward a more exploitative choice policy favoring high-value options. In contrast, pOVX females did not show this phase-dependent increase, suggesting continued use of a more exploratory strategy. To identify a neural correlate, we performed whole-cell patch clamp recordings within the dorsomedial striatum (DMS), a region implicated in regulating action selection and explore/exploit choice policy. Dopamine receptor type 2-expressing (D2R) indirect pathway spiny projection neurons (iSPNs) were significantly more intrinsically excitable in pOVX females compared to sham-operated and unmanipulated controls. Finally, we tested whether increasing D2R(+) iSPN excitability was sufficient to produce a similar choice-policy phenotype. In intact female mice, chemogenetic activation increased exploratory choice during reversal learning, resembling the pattern observed following pOVX. Together, these data show that pOVX is associated with long-lasting changes in DMS iSPN intrinsic excitability and reversal-phase choice policy, while experimentally increasing DMS iSPN activity is sufficient to produce a similar behavioral pattern.

Hypogonadism in males is associated with reduced motivation, fatigue, and decreased goal-directed behavior, yet the neural mechanisms underlying these changes remain poorly understood. Dopamine signaling within the nucleus accumbens (NAc) plays a central role in regulating effort-based decision making, and here we tested the hypothesis that loss of testicular hormones alters mesoaccumbal dopamine function to increase sensitivity to effort-related costs. Male mice underwent orchiectomy (ORX) either before puberty onset or in adulthood and were tested in a progressive ratio 1 closed economy (PR1-CE) task. Dopamine-related function was probed using systemic haloperidol administration and high-performance liquid chromatography to measure dopamine and its metabolites, while whole-cell recordings assessed the intrinsic excitability of NAc spiny projection neurons (SPNs). ORX increased sensitivity to effort costs, reflected by a shift toward energy-efficient responding while maintaining food intake. These behavioral changes were accompanied by reduced responsiveness to haloperidol. Postpubertal ORX increased NAc dopamine content and reduced metabolite-to-dopamine ratios, whereas prepubertal ORX did not alter dopamine neurochemistry. Prepubertal ORX selectively reduced excitability of NAc core D1R[+] SPNs, whereas postpubertal ORX increased excitability across both D1R[+] and D1R[-] populations. Together, these findings demonstrate that ORX increases effort cost sensitivity and is associated with alterations in mesoaccumbal circuit function. Although similar behavioral phenotypes emerged following pre- and postpubertal ORX, distinct neurochemical and cellular adaptations suggest that timing may shape the neural response to ORX. These results provide insight into the circuit mechanisms that may underlie altered motivation following testicular hormone loss.

Rats can either use place memory, response memory or rely on a single cue to navigate their environment. Which navigation strategy a female rat is biased towards is influenced by circulating levels of ovarian hormones. Hormonal contraceptive use is typically associated with changes in circulating levels of endogenous ovarian hormones. The aim of the current study was to examine the effects of synthetic hormones used in hormonal contraceptives on navigation strategies. A total of 61 gonadally intact female rats were tested in two Morris water maze tasks. Rats were administered ethinyl estradiol (EE; 10 μg/kg; n = 10), levonorgestrel (LNG; 20 μg/kg, n = 10), a combination of both EE and LNG (10 μg/kg and 20 μg/kg, n = 10), or vehicle control (n = 31). Controls were tested during either proestrus (n = 10), estrus (n = 11) or diestrus (n = 10). In the place vs. response task, proestrus females exhibited an initial place memory bias while estrus females exhibited an initial response memory bias (OR = 18). However, all groups, apart from the EE + LNG group, eventually spent more time in the place quadrant (η[2] = 0.53), suggesting a corrective shift towards place memory when unable to locate the platform. In the cue task, all groups, apart from the EE + LNG, showed an initial bias to the other quadrant (η[2] = 0.41). This initial bias was abolished in all groups, apart from proestrus females, by the end of the probe. The EE + LNG group failed to exhibit a bias for any of the navigation strategies throughout, suggesting that this formulation of combined EE + LNG may impede memory bias formation.

Filial imprinting in precocial birds provides an unusually tractable example of how a brief early-life experience becomes a durable behavioral commitment. Decades of work in the domestic chick have identified the intermediate medial mesopallium (IMM), thyroid-hormone-dependent regulation of the sensitive period, rapid kinase and translational signaling, receptor and synaptic remodeling, later transcriptional divergence, and distributed retrieval networks. What remains unresolved is how these events relate across scales. Here the ARCH × Φ framework is extended into a recursively coupled execution-encoding architecture. At the execution layer, orienting and approach require the joint action of neural architecture (A), behavioral drive (D), stimulus context (C), and an immediate permissive state (Φ). At the encoding layer, activity generated by successful execution engages intracellular mechanisms that can reconfigure a multidimensional neural substrate. The resulting substrate change, rather than persistence of the original gate, alters future execution and learning capacity. In the chick, the sensitive-period component of Φ is treated operationally as an effective writability state with experimentally separable control points, including rapid thyroid-hormone signaling, GABAergic balance, and AKT/mTORC1-dependent translational capacity. This formulation explicitly accommodates evidence that the rapid imprinting-permissive action of T3 is non-genomic. Chromatin regulation is retained only as a plausible downstream stabilization mechanism whose direct role in chick IMM remains untested. The account further distinguishes the transient gate from the persistent substrate written while that gate is open, reinterprets priming as persistence of that substrate rather than prolonged T3 signaling, and represents encoding as signed, multidimensional reconfiguration rather than monotonic accumulation. The model generates testable predictions concerning gate control, modality-specific implementation, structural reorganization, cross-scale covariance, and retrieval-network redistribution. Filial imprinting is thereby treated as a special case of a broader biological problem: how transient permissiveness allows experience to rewrite the substrate on which future behavior is executed.

A career in science can follow a linear path or might proceed with many unexpected twists and turns. Junior scientists can be discouraged but, more often than not, talent and perseverance create opportunities that lead to a fulfilling career. Patience also keeps open the door for serendipity. It is also the case that a life of curiosity and experimentation plants many seeds along the way in the form of ideas, unexpected hypothesis-bending data, and supportive collegial relationships. These kernels can germinate quickly, mature slowly over a lifetime or they may lay quiescent only to reappear productively many years later. As an example of these processes in action, in this essay, I describe my career as a lab and field behavioral neuroendocrinologist, the way serendipity steered my path forward and the way early life events sprouted into the sturdy trunks that supported my scientific productivity. This Lifetime Achievement Award is the result of many serendipitous events, and, since most of these involve avian neuroendocrinology, it is highly appropriate that Danny Lehrman's name is also being honored. I am proud to be associated with his life and influence.

The regulation of feeding behavior, particularly the timely cessation of food intake, is essential for maintaining energy balance. In mammals, the gut-derived hormone peptide YY (PYY) plays an important role in short-term satiety signaling, with circulating concentrations increasing rapidly after meals to suppress further food intake. In non-mammalian vertebrates, however, the role of PYY in satiety signaling remains poorly understood. The aim of the present study was to test the hypothesis that circulating PYY functions as a short-term satiety signal in birds, analogous to its established role in mammals. We compared preprandial and postprandial circulating PYY concentrations in adult zebra finches (Taeniopygia guttata) that were either food-restricted for 20 days or fed ad libitum. In addition, we quantified feeding motivation, measured as latency to initiate feeding, and food consumption to assess whether variation in circulating PYY was associated with feeding behavior. Contrary to our predictions, circulating PYY concentrations did not increase following feeding, did not significantly differ between food-restricted and ad libitum birds, and were unrelated to either feeding latency or food consumption. Collectively, these findings fail to support the hypothesis that PYY functions as a conserved short-term satiety signal in zebra finches. Instead, our results suggest that the role of PYY in zebra finches may differ from the mammalian pattern and highlight the need for additional comparative studies in birds.

Thyroid hormones regulate embryonic and fetal neurodevelopment, with the maternal thyroid gland exclusively producing these hormones for the first half of gestation and then a combination of maternal and fetal production occurring during the second half of gestation. Hypothyroidism during pregnancy is common in humans, particularly due to the additional demand put on the thyroid gland as pregnancy proceeds. Epidemiological studies have linked maternal hypothyroidism to an increased risk of attention-deficit/hyperactivity disorder and autism spectrum disorder diagnosis in these children, as well as cognitive deficits and delays. Rodent models have been extensively used to model developmental hypothyroidism and study the long-term effects on offspring. Increases in activity, reductions in anxiety, cognitive impairments, and social alterations have been observed. In this review, I discuss the current understanding of the organizational impacts of hypothyroidism on activity, affective behaviors, cognition, and social behaviors in humans and animal models, paying special attention to critical periods that may underlie these effects. I also review potential interactions between thyroid hormones and steroid hormones known to be important for organization of the brain and behavior during perinatal and adolescent development. Understanding the effects of developmental hypothyroidism is critical, as early developmental exposure to many endocrine-disrupting chemicals may alter behavior through reducing thyroid hormone signaling, and the final section of the paper reviews these interactions. Understanding the organizational effects of thyroid hormones is important for decisions related to screening and interventions during pregnancy.

This paper reviews evidence that neurons in the anterior cingulate cortex (ACC) and anterior insular cortex (AI) are involved in the production of altruistic behaviors. But because so many other cognitive and behavioral functions have been ascribed to ACC and AI, one must ask: how might mechanisms producing altruistic behaviors be distinguished from those for other functions? We hypothesize that oxytocin actions in ACC and AI can provide mechanisms fostering altruistic behaviors. Secondarily, we hypothesize that von Economo neurons participate in oxytocin's support of altruistic behaviors.

Sex differences in circulating androgens are well-known to organize and activate neural and behavioral sex differences of traditional animal models, but much less is known about the consequences of intrasexual differences in androgens. One approach to this question is studying the effects of hyperandrogenism in females. Hyperandrogenism is associated with several endocrine conditions affecting women, with polyendocrine metabolic ovarian syndrome (PMOS) being the most common during reproductive years. PMOS symptoms often emerge around puberty, raising the possibility of organizational effects of hyperandrogenism on neurobehavioral phenotype. Using a mouse model of PMOS, we examined how the timing of symptom induction by 5α-dihydrotestosterone (DHT) treatment affects androgen-linked sociosexual behavioral phenotype. Female mice received DHT or vehicle treatment at peripuberty (PND21) and again in adulthood (PND60), generating four treatment groups with distinct developmental treatment histories. Behavioral testing assessed social preference, stereotyped/repetitive behaviors and partnered social interactions following the first and second androgen treatment. Brain FOS following partnered interaction with an age-matched, unfamiliar female was also measured. Peripubertal DHT treatment accelerated pubertal onset, as indicated by earlier vaginal opening and increased body weight. Androgen treatment had no effect on stereotyped/repetitive behavior or FOS expression but peripubertal androgen treatment altered exploratory activity during adult social preference tests, rather than social preference per se. In partnered interaction tests, both peripubertal and adult androgens increased masculine sexual approach responses, including mounting, with minimal effects on social behavior. These results are consistent with other evidence that peripubertal androgenic mechanisms can organize neurobehavioral phenotypes.

Tuco-tucos (Ctenomys coludo) are Neotropical rodents that inhabit the extreme photic environment of the subterranean, thus being intriguing models for chronobiological studies of circadian and seasonal rhythms. Here we characterized day/night profiles of plasma melatonin and glucocorticoids along with their activity/rest rhythms from freshly caught animals during two seasons. Animals were live-trapped in their native Monte Desert (Argentina) during summer (n = 27) and winter (n = 18), housed under constant dark conditions with wheel-running activity recording prior to sample collection. Sampling occurred at six timepoints across day and night to obtain cross-sectional data. Unlike typical lab-based seasonal studies using artificial photoperiods, our approach captures the complexity of environmental cycles by studying wild animals exposed to the full array of environmental variations across seasons. Melatonin, cortisol and corticosterone were analyzed via ELISA. Melatonin levels showed circadian rhythmicity with higher levels during subjective night. Results revealed higher levels of cortisol secretion during subjective night, consistent with the profile of a nocturnal-active animal. Cortisol levels were 25 to 50 times higher than corticosterone. These findings provide the first circadian melatonin and glucocorticoid baseline for C. coludo in two seasons paving the way for future work on their endocrine rhythms and interplay with activity/rest rhythms and other circadian patterns.

Emotional experience and the regulation thereof are typically studied using picture inventories or short films to induce and modify affective states. These approaches, however, lack ecological validity due to their passive and receptive nature. Recent innovations in virtual reality and mobile neurophysiological technologies have enabled researchers to study the behavioral and neural correlates of more ecologically valid emotional responses. In this preregistered study, 58 healthy participants were randomly assigned to either use cognitive reappraisal (intervention) or to immerse themselves in their senses and surroundings (control) while walking across a wooden plank suspended 80 stories above the ground in virtual reality. We measured subjective fear ratings, salivary alpha amylase and cortisol levels, as well as frontal brain asymmetries, captured using mobile electroencephalography (EEG). Across both conditions, we found decisive evidence of increased subjective fear and salivary alpha amylase, a marker of sympathetic activation. However, we found no increase in cortisol levels following the task suggesting that subjective fear alone is not sufficient to trigger a cortisol response. In contrast to our hypotheses, the reappraisal group did not show any difference compared to the control group for neither emotional, endocrine nor neural measures. On the one hand, our findings may suggest that reappraisal might not be a suitable strategy to regulate realistic and intensely frightening situations. On the other hand, further analyses also indicated that the control group may have also regulated their emotions due to increased mindfulness of their inner states and their environment. Future studies are needed to confirm these observations and ascertain the efficacy of cognitive reappraisal on fear in realistic settings.