Urban and rural male song sparrows (Melospiza melodia) differ in territorial aggression and activation of vasotocin neurons in response to song challenge.

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.

Corticosterone and immune responses to dehydration in squamate reptiles.

Many environments present some degree of seasonal water limitations; organisms that live in such environments must be adapted to survive periods without permanent water access. Often this involves the ability to tolerate dehydration, which can have adverse physiological effects and is typically considered a physiological stressor. While having many functions, the hormone corticosterone (CORT) is often released in response to stressors, yet increasing plasma CORT while dehydrated could be considered maladaptive, especially for species that experience predictable bouts of dehydration and have related coping mechanisms. Elevating CORT could reduce immunocompetence and have other negative physiological effects. Thus, such species likely have CORT and immune responses adapted to experiencing seasonal droughts. We evaluated how dehydration affects CORT and immune function in eight squamate species that naturally experience varied water limitation. We tested whether hydric state affected plasma CORT concentrations and aspects of immunocompetence (lysis, agglutination, bacterial killing ability and white blood cell counts) differently among species based on how seasonally water limited they are and whether this is constrained by phylogeny. The species represented four familial pairs, with one species of each pair inhabiting environments with frequent access to water and one naturally experiencing extended periods (>30 days) with no access to standing water. The effects of dehydration on CORT and immunity varied among species. Increases in CORT were generally not associated with reduced immunocompetence, indicating CORT and immunity might be decoupled in some species. Interspecies variations in responses to dehydration were more clearly grouped by phylogeny than by habitat type.

Structure of human endo-α-1,2-mannosidase (MANEA), an antiviral host-glycosylation target.

Mammalian protein N-linked glycosylation is critical for glycoprotein folding, quality control, trafficking, recognition, and function. N-linked glycans are synthesized from Glc3Man9GlcNAc2 precursors that are trimmed and modified in the endoplasmic reticulum (ER) and Golgi apparatus by glycoside hydrolases and glycosyltransferases. Endo-α-1,2-mannosidase (MANEA) is the sole endo-acting glycoside hydrolase involved in N-glycan trimming and is located within the Golgi, where it allows ER-escaped glycoproteins to bypass the classical N-glycosylation trimming pathway involving ER glucosidases I and II. There is considerable interest in the use of small molecules that disrupt N-linked glycosylation as therapeutic agents for diseases such as cancer and viral infection. Here we report the structure of the catalytic domain of human MANEA and complexes with substrate-derived inhibitors, which provide insight into dynamic loop movements that occur on substrate binding. We reveal structural features of the human enzyme that explain its substrate preference and the mechanistic basis for catalysis. These structures have inspired the development of new inhibitors that disrupt host protein N-glycan processing of viral glycans and reduce the infectivity of bovine viral diarrhea and dengue viruses in cellular models. These results may contribute to efforts aimed at developing broad-spectrum antiviral agents and help provide a more in-depth understanding of the biology of mammalian glycosylation.

The human liver microenvironment shapes the homing and function of CD4+ T-cell populations.

OBJECTIVE: Tissue-resident memory T cells (TRM) are vital immune sentinels that provide protective immunity. While hepatic CD8+ TRM have been well described, little is known about the location, phenotype and function of CD4+ TRM. DESIGN: We used multiparametric flow cytometry, histological assessment and novel human tissue coculture systems to interrogate the ex vivo phenotype, function and generation of the intrahepatic CD4+ T-cell compartment. We also used leukocytes isolated from human leukocyte antigen (HLA)-disparate liver allografts to assess long-term retention. RESULTS: Hepatic CD4+ T cells were delineated into three distinct populations based on CD69 expression: CD69-, CD69INT and CD69HI. CD69HICD4+ cells were identified as tissue-resident CD4+ T cells on the basis of their exclusion from the circulation, phenotypical profile (CXCR6+CD49a+S1PR1-PD-1+) and long-term persistence within the pool of donor-derived leukcoocytes in HLA-disparate liver allografts. CD69HICD4+ T cells produced robust type 1 polyfunctional cytokine responses on stimulation. Conversely, CD69INTCD4+ T cells represented a more heterogenous population containing cells with a more activated phenotype, a distinct chemokine receptor profile (CX3CR1+CXCR3+CXCR1+) and a bias towards interleukin-4 production. While CD69INTCD4+ T cells could be found in the circulation and lymph nodes, these cells also formed part of the long-term resident pool, persisting in HLA-mismatched allografts. Notably, frequencies of CD69INTCD4+ T cells correlated with necroinflammatory scores in chronic hepatitis B infection. Finally, we demonstrated that interaction with hepatic epithelia was sufficient to generate CD69INTCD4+ T cells, while additional signals from the liver microenvironment were required to generate liver-resident CD69HICD4+ T cells. CONCLUSIONS: High and intermediate CD69 expressions mark human hepatic CD4+ TRM and a novel functionally distinct recirculating population, respectively, both shaped by the liver microenvironment to achieve diverse immunosurveillance.

Hypothalamic-pituitary-adrenal axis regulation and organization in urban and rural song sparrows.

Urban habitats present animals with persistent disturbances and acute stressors not present in rural habitats or present at significantly lower levels. Differences in the glucocorticoid stress response could underlie colonization of these novel habitats. Despite urban habitats characterization as more stressful, previous comparisons of urban and rural birds have failed to find consistent differences in baseline and stress induced glucocorticoid levels. Another aspect of glucocorticoid regulation that could underlie an animal's ability to inhabit novel habitats, but has yet to be well examined, is more efficient termination of the glucocorticoid stress response which would allow birds in urban habitats to recover more quickly after a disturbance. The glucocorticoid stress response is terminated by negative feedback achieved primarily through their binding of receptors in the hippocampus and hypothalamus and subsequent decreased synthesis and release from the adrenals. We investigated if male song sparrows (Melospiza melodia) in urban habitats show more efficient termination of the glucocorticoid stress response than their rural counterparts using two approaches. First, we measured glucocorticoid receptor, mineralocorticoid receptor and 11ß-HSD2 (an enzyme that inactivates corticosterone) mRNA expression in negative feedback targets of the brain (the hippocampus and hypothalamus) as a proxy measure of sensitivity to negative feedback. Second, we measured plasma corticosterone levels after standardized restraint and again following a challenge with the synthetic glucocorticoid, dexamethasone, as a means of assessing how quickly birds decreased glucocorticoid synthesis and release. Though there were no differences in the hypothalamus of urban and rural song sparrows, urban birds had lower glucocorticoid receptor and 11ß-HSD2 mRNA expression in the hippocampus. Further, urban and rural birds had similar reductions in corticosterone following the dexamethasone challenge, suggesting that they do not differ in how quickly they decrease glucocorticoid synthesis and release. Thus, urban and rural song sparrows display similar termination of the glucocorticoid stress response even though urban birds have decreased hippocampal glucocorticoid receptor and 11ß-HSD2 abundance.

An indolent cause of high-output heart failure in end-stage kidney disease-Application of the Nicoladoni-Israel-Branham test: A case report.

BACKGROUND: A hemodynamically significant arteriovenous fistula (AVF) in end-stage kidney disease (ESKD) causes a high flow state, resulting in pathologic cardiovascular remodeling, and deserves timely clinical recognition. CASE: A 55-year-old woman with history of ESKD with deceased donor kidney transplant with failing graft function and baseline creatinine of 2.8 mg/dl presented to the clinic with nocturnal cough, orthopnea, dyspnea on exertion and pedal edema. Physical exam was notable for large, aneurysmal right brachial AVF. Transthoracic echocardiography (TTE) revealed left ventricular (LV) enlargement and hypertrophy and elevated cardiac output (CO) of 10 L/min, raising a clinical concern for high-output heart failure. DECISION MAKING: A non-invasive assessment of the hemodynamic significance of the AVF was performed using a TTE. During temporary occlusion of the AVF, it was determined that about 27% of the resting CO was attributed to the AVF, suggesting hemodynamic significance. Nicoladoni-Israel-Branham sign was negative as there was no change in patient's heart rate, but this was potentially attributed to beta-blockade and chronic loading conditions. She underwent AVF banding and 2-month later her presenting symptoms resolved, and a TTE showed a decrease in resting CO of 7.6 L/min with normalization of LV size. CONCLUSION: This case highlights several teaching points. Firstly, in patients with ESKD, a large AVF can contribute to a high CO state resulting in maladaptive cardiovascular remodeling. Secondly, TTE evaluation of the hemodynamic contribution of an AVF can be performed with the application of the Nicoladoni-Israel-Branham sign. Finally, some experts recommend pre-emptive banding or ligation of AVF after successful kidney transplantation as this has been shown to have symptomatic and cardiovascular benefits.

Supramolecular Cylinders Target Bulge Structures in the 5' UTR of the RNA Genome of SARS-CoV-2 and Inhibit Viral Replication*.

The untranslated regions (UTRs) of viral genomes contain a variety of conserved yet dynamic structures crucial for viral replication, providing drug targets for the development of broad spectrum anti-virals. We combine in vitro RNA analysis with molecular dynamics simulations to build the first 3D models of the structure and dynamics of key regions of the 5' UTR of the SARS-CoV-2 genome. Furthermore, we determine the binding of metallo-supramolecular helicates (cylinders) to this RNA structure. These nano-size agents are uniquely able to thread through RNA junctions and we identify their binding to a 3-base bulge and the central cross 4-way junction located in stem loop 5. Finally, we show these RNA-binding cylinders suppress SARS-CoV-2 replication, highlighting their potential as novel anti-viral agents.

Genetic inheritance and environment determine endocrine plasticity to urban living.

As urban areas continue to expand globally, understanding how and why species respond to novel habitats becomes increasingly important. Knowledge of the mechanisms behind observed phenotypic changes in urban animals will enable us to better evaluate the impact of urbanization on current and future generations of wildlife. Physiological changes, such as those involved in the endocrine stress response, may allow individuals to inhabit and thrive in urbanized areas, but it is currently unknown how these changes arise in natural populations. In this study, we performed a four-way cross-foster experiment in free-living house wren chicks, Troglodytes aedon, to disentangle whether differences in baseline corticosterone between urban and rural individuals are a result of genetic and/or plastic mechanisms during development. We found that urban chicks already had higher corticosterone levels than their rural counterparts on the day they hatched, which suggests a possible genetic component to the corticosterone phenotype. However, rural offspring that were moved to an urban environment significantly increased their corticosterone levels, mimicking those of urban offspring. Our findings suggest that, although differences in baseline corticosterone concentrations between urban and rural individuals may have a genetic component, plasticity plays a pivotal role and can modify the corticosterone phenotype in response to the environment experienced in the first two weeks of life.

MerTK expressing hepatic macrophages promote the resolution of inflammation in acute liver failure.

OBJECTIVE: Acute liver failure (ALF) is characterised by overwhelming hepatocyte death and liver inflammation with massive infiltration of myeloid cells in necrotic areas. The mechanisms underlying resolution of acute hepatic inflammation are largely unknown. Here, we aimed to investigate the impact of Mer tyrosine kinase (MerTK) during ALF and also examine how the microenvironmental mediator, secretory leucocyte protease inhibitor (SLPI), governs this response. DESIGN: Flow cytometry, immunohistochemistry, confocal imaging and gene expression analyses determined the phenotype, functional/transcriptomic profile and tissue topography of MerTK+ monocytes/macrophages in ALF, healthy and disease controls. The temporal evolution of macrophage MerTK expression and its impact on resolution was examined in APAP-induced acute liver injury using wild-type (WT) and Mer-deficient (Mer-/-) mice. SLPI effects on hepatic myeloid cells were determined in vitro and in vivo using APAP-treated WT mice. RESULTS: We demonstrate a significant expansion of resolution-like MerTK+HLA-DRhigh cells in circulatory and tissue compartments of patients with ALF. Compared with WT mice which show an increase of MerTK+MHCIIhigh macrophages during the resolution phase in ALF, APAP-treated Mer-/- mice exhibit persistent liver injury and inflammation, characterised by a decreased proportion of resident Kupffer cells and increased number of neutrophils. Both in vitro and in APAP-treated mice, SLPI reprogrammes myeloid cells towards resolution responses through induction of a MerTK+HLA-DRhigh phenotype which promotes neutrophil apoptosis and their subsequent clearance. CONCLUSIONS: We identify a hepatoprotective, MerTK+, macrophage phenotype that evolves during the resolution phase following ALF and represents a novel immunotherapeutic target to promote resolution responses following acute liver injury.

The Reactive Oxygen Species-Mitophagy Signaling Pathway Regulates Liver Endothelial Cell Survival During Ischemia/Reperfusion Injury.

Ischemia/reperfusion injury (IRI) is the main cause of complications following liver transplantation. Reactive oxygen species (ROS) were thought to be the main regulators of IRI. However, recent studies demonstrate that ROS activate the cytoprotective mechanism of autophagy promoting cell survival. Liver IRI initially damages the liver endothelial cells (LEC), but whether ROS-autophagy promotes cell survival in LEC during IRI is not known. Primary human LEC were isolated from human liver tissue and exposed to an in vitro model of IRI to assess the role of autophagy in LEC. The role of autophagy during liver IRI in vivo was assessed using a murine model of partial liver IRI. During IRI, ROS specifically activate autophagy-related protein (ATG) 7 promoting autophagic flux and the formation of LC3B-positive puncta around mitochondria in primary human LEC. Inhibition of ROS reduces autophagic flux in LEC during IRI inducing necrosis. In addition, small interfering RNA knockdown of ATG7 sensitized LEC to necrosis during IRI. In vivo murine livers in uninjured liver lobes demonstrate autophagy within LEC that is reduced following IRI with concomitant reduction in autophagic flux and increased cell death. In conclusion, these findings demonstrate that during liver IRI ROS-dependent autophagy promotes the survival of LEC, and therapeutic targeting of this signaling pathway may reduce liver IRI following transplantation.

Territorial aggression in urban and rural Song Sparrows is correlated with corticosterone, but not testosterone.

Urban songbirds of several species more vigorously defend their territories in response to conspecific song playback than do their rural counterparts, but the hormonal basis of this behavioral difference is unclear. It is well established in vertebrates that both testosterone and corticosterone affect the intensity of territoriality. Previous studies have found no evidence that initial (i.e., immediately following territorial challenge, but prior to restraint) plasma testosterone accounts for the elevated territorial aggression of urban birds. Determining if testosterone still contributes to urban-rural differences in territoriality requires also assessing males' abilities to transiently increase plasma testosterone (in response to an injection of gonadotropin-releasing hormone). We tested whether these hormones are correlated with the territorial response to conspecific song playback in urban and rural male Song Sparrows (Melospiza melodia) in Montgomery County, Virginia. We found that the elevated territorial aggression of urban sparrows was not related to variation in either initial plasma testosterone or the ability to transiently increase testosterone. In contrast, despite no overall habitat difference in initial corticosterone, levels of this hormone were positively correlated with territoriality in urban and rural sparrows. Furthermore, for a given level of corticosterone, urban sparrows were more territorially aggressive. Our findings suggest that initial corticosterone may either play a role in the regulation of persistent differences in territorial behavior between free-ranging urban and rural male Song Sparrows or be affected by the intensity of behavioral response to territorial challenge.

Hormonally mediated effects of artificial light at night on behavior and fitness: linking endocrine mechanisms with function.

Alternation between day and night is a predictable environmental fluctuation that organisms use to time their activities. Since the invention of artificial lighting, this predictability has been disrupted and continues to change in a unidirectional fashion with increasing urbanization. As hormones mediate individual responses to changing environments, endocrine systems might be one of the first systems affected, as well as being the first line of defense to ameliorate any negative health impacts. In this Review, we first highlight how light can influence endocrine function in vertebrates. We then focus on four endocrine axes that might be affected by artificial light at night (ALAN): pineal, reproductive, adrenal and thyroid. Throughout, we highlight key findings, rather than performing an exhaustive review, in order to emphasize knowledge gaps that are hindering progress on proposing impactful and concrete plans to ameliorate the negative effects of ALAN. We discuss these findings with respect to impacts on human and animal health, with a focus on the consequences of anthropogenic modification of the night-time environment for non-human organisms. Lastly, we stress the need for the integration of field and lab experiments as well as the need for long-term integrative eco-physiological studies in the rapidly expanding field of light pollution.

Commensal-derived OMVs elicit a mild proinflammatory response in intestinal epithelial cells.

Under normal physiological conditions, the intestinal immunity remains largely hyporesponsive to the commensal microbiota, yet also retains the inherent ability to rapidly respond to pathogenic antigens. However, immunomodulatory activities of extracellular products from commensal bacteria have been little studied, with previous investigations generally utilizing the live bacterium to study microbiota-epithelial interactions. In this study, we demonstrate that extracellular products of a commensal bacterium, Escherichia coli C25, elicit a moderate release of proinflammatory IL-8 and stimulate transcriptional up-regulation of Toll-like receptors (TLRs) in intestinal epithelial cell lines HT29-19A and Caco-2. Additionally, we show that removal of outer membrane vesicles (OMVs) reduces the proinflammatory effect of secreted products from E. coli C25. Furthermore, we show that isolated OMVs have a dose-dependent proinflammatory effect on intestinal epithelial cells (IECs). Interestingly, a relatively high concentration (40 µg ml-1 protein) of OMVs had no significant regulatory effects on TLR mRNA expression in both cell lines. Finally, we also demonstrate that pre-incubation with E. coli C25-derived OMVs subsequently inhibited the internalization of the bacterium itself in both cell lines. Taken together, our results suggest that commensal-derived extracellular products, in particular OMVs, could significantly contribute to intestinal homeostasis. We also demonstrate a unique interaction between commensal-derived OMVs and host cells.

Dehydration enhances multiple physiological defense mechanisms in a desert lizard, Heloderma suspectum.

The physiological challenges associated with dehydration can induce an increase in plasma glucocorticoid concentrations, a response thought to provide the mechanism for dehydration suppressing immune function. However, a comprehensive examination of the inter-relationship of dehydration, stress and immune function has not been conducted within a single species. We previously demonstrated that Gila monsters (Heloderma suspectum), which inhabit a xeric environment with a predictable seasonal drought, have enhanced measures of innate immunity when dehydrated. These results suggest that, in this species, dehydration may not induce a glucocorticoid response, but, instead, enhances physiological defense mechanisms. To explore this possibility, we examined multiple measures of innate immunity as well as initial and reactive plasma concentrations of glucocorticoids in captive and free-ranging Gila monsters at various hydration states. Our results show that, in this species, dehydration alone does not cause a substantial increase in plasma glucocorticoids, and we provide broader evidence that dehydration enhances defensive mechanisms including stress reactivity and various measures of innate immune function. These findings suggest that physiological responses to dehydration may depend heavily on an organism's ecology. More research on the effects of dehydration on the glucocorticoid response and immunity will help clarify the interactive roles they play in response to hydration challenges and whether adaptations to water-limited environments influence these interactions.

Stressful city sounds: glucocorticoid responses to experimental traffic noise are environmentally dependent.

A major challenge in urban ecology is to identify the environmental factors responsible for phenotypic differences between urban and rural individuals. However, the intercorrelation between the factors that characterize urban environments, combined with a lack of experimental manipulations of these factors in both urban and rural areas, hinder efforts to identify which aspects of urban environments are responsible for phenotypic differences. Among the factors modified by urbanization, anthropogenic sound, particularly traffic noise, is especially detrimental to animals. The mechanisms by which anthropogenic sound affects animals are unclear, but one potential mechanism is through changes in glucocorticoid hormone levels. We exposed adult house wrens, Troglodytes aedon, to either traffic noise or pink noise (a non-traffic noise control). We found that urban wrens had higher initial (pre-restraint) corticosterone than rural wrens before treatment, and that traffic noise elevated initial corticosterone of rural, but not urban, wrens. By contrast, restraint stress-induced corticosterone was not affected by noise treatment. Our results indicate that traffic noise specifically contributes to determining the glucocorticoid phenotype, and suggest that glucocorticoids are a mechanism by which anthropogenic sound causes phenotypic differences between urban and rural animals.

Agonistic urban birds: elevated territorial aggression of urban song sparrows is consistent within a breeding period.

Urban birds often more vigorously defend their territories during simulated intrusions than do their rural counterparts, but the factors responsible remain unclear. To address this issue, we investigated whether the disparity in territorial aggression of urban and rural male song sparrows, Melospiza melodia, is individually consistent within a breeding period. Additionally, to better understand the physiological and ecological factors underlying this behavioural difference, we examined whether territoriality was associated with plasma testosterone, a hormone that contributes to elevated aggression in vertebrates, and/or conspecific density, a factor often positively related to aggression. The urbanization-related difference in territoriality was individually consistent within a breeding period. However, the elevated territorial aggression of urban birds was not associated with plasma testosterone and, counter to our predictions, conspecific density was lower in urban compared with rural areas. We suggest that other aspects of testosterone signalling and features of the socio-ecological environment, such as the availability of breeding sites, may underlie increased territorial aggression in urban birds.

Endocrine, metabolic, and behavioral effects of and recovery from acute stress in a free-ranging bird.

Acute stress in vertebrates generally stimulates the hypothalamo-pituitary-adrenal axis and is often associated with multiple metabolic changes, such as increased gluconeogenesis, and with behavioral alterations. Little information is available, especially in free-ranging organisms, on the duration of these reversible effects once animals are no longer exposed to the stressor. To investigate this question, we exposed free-ranging adult male Rufous-winged Sparrows, Peucaea carpalis, in breeding condition to a standard protocol consisting of a social challenge (conspecific song playback) followed with capture and restraint for 30min, after which birds were released on site. Capture and restraint increased plasma corticosterone (CORT) and decreased plasma testosterone (T), glucose (GLU), and uric acid (UA). In birds that we recaptured the next day after exposure to conspecific song playback, plasma CORT and UA levels no longer differed from levels immediately after capture the preceding day. However, plasma T was similar to that measured after stress exposure the preceding day, and plasma GLU was markedly elevated. Thus, exposure to social challenge and acute stress resulted in persistent (⩾24h) parameter-specific effects. In recaptured sparrows, the territorial aggressive response to conspecific song playback, as measured by song rate and the number of flights over the song-broadcasting speakers, did not, however, differ between the first capture and the recapture, suggesting no proximate functional association between plasma T and conspecific territorial aggression. The study is the first in free-ranging birds to report the endocrine, metabolic, and behavioral recovery from the effects of combined social challenge and acute stress.

The ecological and physiological bases of variation in the phenology of gonad growth in an urban and desert songbird.

Birds often adjust to urban areas by advancing the timing (phenology) of vernal gonad growth. However, the ecological and physiological bases of this adjustment are unclear. We tested whether the habitat-related disparity in gonad growth phenology of male Abert's towhees, Melozone aberti, is due to greater food availability in urban areas of Phoenix, Arizona USA or, alternatively, a habitat-related difference in the phenology of key food types. To better understand the physiological mechanism underlying variation in gonad growth phenology, we compared the activity of the reproductive system at all levels of hypothalamo-pituitary-gonadal (HPG) axis. We found no habitat-associated difference in food availability (ground arthropod biomass), but, in contrast to the seasonal growth of leaves on desert trees, the leaf foliage of urban trees was already developed at the beginning of our study. Multiple estimates of energetic status did not significantly differ between the non-urban and urban towhees during three years that differed in the habitat-related disparity in gonad growth and winter precipitation levels. Thus, our results provide no support for the hypothesis that greater food abundance in urban areas of Phoenix drives the habitat-related disparity in gonad growth phenology in Abert's towhees. By contrast, they suggest that differences in the predictability and magnitude of change in food availability between urban and desert areas of Phoenix contribute to the observed habitat-related disparity in gonad growth. Endocrine responsiveness of the gonads may contribute to this phenomenon as desert - but not urban - towhees had a marked plasma testosterone response to GnRH challenge.

The seasonal glucocorticoid response of male Rufous-winged Sparrows to acute stress correlates with changes in plasma uric acid, but neither glucose nor testosterone.

We sought to clarify functional relationships between baseline and acute stress-induced changes in plasma levels of the stress hormone corticosterone (CORT) and the reproductive hormone testosterone (T), and those of two main metabolites, uric acid (UA) and glucose (GLU). Acute stress in vertebrates generally stimulates the secretion of glucocorticoids, which in birds is primarily CORT. This stimulation is thought to promote behavioral and metabolic changes, including increased glycemia. However, limited information in free-ranging birds supports the view that acutely elevated plasma CORT stimulates glycemia. Acute stress also often decreases the secretion of reproductive hormones (e.g., T in males), but the role of CORT in this decrease and the contribution of T to the regulation of plasma GLU remain poorly understood. We measured initial (pre-stress) and acute stress-induced plasma CORT and T as well as GLU in adult male Rufous-winged Sparrows, Peucaea carpalis, sampled during the pre-breeding, breeding, post-breeding molt, and non-breeding stages. Stress increased plasma CORT and the magnitude of this increase did not differ across life history stages. The stress-induced elevation of plasma CORT was consistently associated with decreased plasma UA, suggesting a role for CORT in the regulation of plasma UA during stress. During stress plasma GLU either increased (pre-breeding), did not change (breeding), or decreased (molt and non-breeding), and plasma T either decreased (pre-breeding and breeding) or did not change (molt and non-breeding). These data provide only partial support to the hypothesis that CORT secretion during acute stress exerts a hyperglycemic action or is responsible for the observed decrease in plasma T taking place at certain life history stages. They also do not support the hypothesis that rapid changes in plasma T influence glycemia.

Beeswax corticosterone implants produce long-term elevation of plasma corticosterone and influence condition.

Glucocorticoids can play a critical role in modulating life-history trade-offs. However, studying the effects of glucocorticoids on life-history often requires experimentally elevating plasma glucocorticoid concentrations for several weeks within normal physiological limits and without repeated handling of the animal. Recently, implants made of beeswax and testosterone (T) were shown to have release dynamics superior to some currently available T implants, and these beeswax implants dissolved, eliminating the need to recapture the animal. We evaluated the utility of beeswax implants containing four different dosages of corticosterone (CORT; the primary glucocorticoid in birds) and their effect on several condition indices in a captive colony of zebra finches (Taeniopygia guttata). The three implants with the greatest CORT doses (0.05, 0.1, and 0.5mg) produced spikes in plasma CORT concentrations 20h after treatment, but were within the limits that zebra finches may normally experience. The 0.5mg CORT implant elevated plasma CORT between typical baseline and restraint stress levels reported in other studies of zebra finches for the entire 35day experiment. Birds in the 0.5mg implant group were heavier, had greater furcular fat scores, and had lower hematocrit than birds in the control and other CORT implant groups. Beeswax CORT implants are a low cost method of elevating plasma CORT for a prolonged time. Furthermore, because there is no need to remove these implants at the end of a study, this method may be amenable to studies of free-ranging animals.