Plasma Corticosterone Response Research Articles

Supplementation with vitamin E does not alter plasma leptin, adiponectin or corticosterone response to different high-fat diets in rats

The aim of the study was to assess if supplementation of high-fat diets with vitamin E influences circulating leptin, adiponectin and corticosterone (Cs) in rats. Forty-eight male rats were divided into 4 groups of 12 rats each, and for 6 weeks fed on 20% (wt/wt)-fat diets. Dietary fat was provided by cod liver oil (CLO), grape seed oil (GO), rape seed oil (RO), or lard (L), enriched with vitamin E (500 mg/kg, +E), or not. Plasma hormone levels were unaffected by vitamin E supplementation. Corticosterone concentrations were, however, higher in RO+E rats compared with non-supplemented RO rats. Fat type had a significant impact on relative plasma adipokine levels, body weight, and body fatness. Specifically, GO and RO exhibited the highest levels of adipokines. Yet, plasma Cs levels did not vary among groups. Our study supports the preventive role of vegetable fats, even if supplied in excess, against adipose tissue deposition and its ramifications in terms of hormone secretion.

Distinct, Time-Dependent Effects of Voluntary Exercise on Circadian and Ultradian Rhythms and Stress Responses of Free Corticosterone in the Rat Hippocampus

Previous work has shown that allowing rats to voluntarily exercise in a running wheel for 4 wk modifies the hypothalamic-pituitary-adrenal axis and behavioral coping responses to stress. To investigate whether long-term voluntary exercise would also affect the free, biologically active fraction of corticosterone in the brain, we conducted an in vivo microdialysis study in the hippocampus of rats. We monitored both the baseline circadian and ultradian patterns of corticosterone in hippocampus dialysates over the diurnal cycle and the responses to forced swim and novelty stress at different stages of exercise. Exercise for 1 d, 2 d, or 1 wk did not affect baseline circadian and ultradian pulse parameters or stress-induced hippocampal free corticosterone concentrations suggesting that acute or short-term periods of exercise do not affect baseline and stress-induced hormone levels. Baseline hormone parameters in 4 wk exercised rats, however, showed significantly increased pulse amplitudes (+108%) and mean free corticosterone levels (+42%) between 1500 and 2100 h but not between 0900 and 1500 h. Surprisingly, although our previous work showed substantial changes in stress-evoked plasma (total) corticosterone responses in long-term exercised animals, no differences in stress-induced hippocampal free hormone responses could be observed between exercised and sedentary animals. This lack of differences was not caused by compensatory changes in plasma corticosteroid-binding-globulin binding levels in exercising rats. Thus, long-term exercising rats show anticipatory increases in glucocorticoid output before the start of the active phase. These rats also reveal the putative existence of a containment mechanism preventing overexposure of the brain to glucocorticoid hormones.

Physiological stress in captive Greater rheas (Rhea americana): Highly sensitive plasma corticosterone response to an ACTH challenge

Up to the present no studies have been conducted either on baseline concentrations of adrenal hormones or on hormonal responses to stress in Greater rhea (Rhea americana) and most ratite species. The aims of this work were to assess the presence of corticosterone in plasma of Greater rhea, to validate a corticosterone 125I-radioimmunoassay for determining corticosterone levels in plasma samples and to study the activation of the adrenal gland after an adrenocorticotrophic hormone (ACTH) challenge. Six captive Greater rhea juveniles of 10months of age received an intravenous ACTH injection. Blood samples were taken at 0min (baseline pre-ACTH levels), and post-injection at 15, 30, 60min and at 24 and 48h. The high pressure liquid chromatography (HPLC) analysis of pooled plasma showed that corticosterone is the glucocorticoid found in the plasma of Greater rhea. Biochemical assays of standard validation (e.g., parallelism, exogenous corticosterone recovery) showed that measurements of corticosterone present in the plasma of the Greater rhea provided by commercial corticosterone 125I-radioimmunoassay were accurate and precise. ACTH challenge induced a more than 40-fold increase in plasma corticosterone at 60min post-ACTH (from 4.0 to 166.5ng/ml, on average). The corticosterone response to ACTH in Greater rhea was higher than is usual in birds, an apparently typical characteristic of ratites.

Gene array analysis of adrenal glands in broiler chickens following ACTH treatment.

BackgroundDifference in adaptability responses to stress has been observed amongst bird species, strains, and individuals. Components of the HPA axis, one of the internal systems involved in homeostasis re-establishment following stress, could play a role in this variability of responses. The aim of the present study was 1) to identify genes involved in the regulation of adrenal activity following ACTH stimulation and 2) to examine adrenal genes differentially expressed in individuals with high and low plasma corticosterone response following ACTH treatment.ResultsAnalysis with 21 K poultry oligo microarrays indicated that ACTH treatment affected the expression of 134 genes. Several transcripts assigned to genes involved in the adrenal ACTH signaling pathway and steroidogenic enzymes were identified as differentially expressed by ACTH treatment. Real-time PCR on 18 selected genes confirmed changes in transcript levels of 11 genes, including MC2R, CREM, Cry, Bmal1, Sqle, Prax1, and StAR. Only 4 genes revealed to be differentially expressed between higher and lower adrenal responders to ACTH treatment.ConclusionThe results from the present study reveal putative candidate genes; their role in regulation of adrenal functions and adaptability to stress should be further investigated.

Subdiaphragmatic Vagotomy Prevents Drinking-Induced Reduction in Plasma Corticosterone in Water-Restricted Rats

Dehydrated rats exhibit a rapid inhibition of the hypothalamic-pituitary-adrenal axis after rehydration. Drinking activates vagal afferents that project to neurons in the nucleus tractus solitarius (NTS). We hypothesized that when dehydrated rats drink, vagal afferents stimulate NTS neurons initiating inhibition of hypothalamic-pituitary-adrenal activity. Experiments assessed NTS activity by measuring Fos expression. Rats were water restricted for 1 or 6 d, limiting access to water to 30 min/d in the morning. Drinking after single or repeated restriction increased Fos, demonstrating increased NTS activity. We next examined the contribution of the vagus by comparing hormonal responses after total subdiaphragmatic vagotomy or sham surgery. Water restriction for 6 d increased plasma arginine vasopressin (AVP), ACTH, and adrenal and plasma corticosterone in both groups. In sham rats, drinking reduced plasma AVP, ACTH, adrenal and plasma corticosterone by 7.5 min. In total subdiaphragmatic vagotomy rats, whereas drinking reduced plasma AVP, ACTH, and adrenal corticosterone, drinking did not reduce plasma corticosterone. To identify the source of vagal activity, hormonal responses to restriction-induced drinking were measured after common hepatic branch vagotomy (HBV). Although pituitary hormonal responses were not affected by HBV, the adrenal and plasma corticosterone responses to water restriction were reduced; in addition, drinking in HBV rats decreased adrenal corticosterone without changing plasma corticosterone. These data indicate that an intact vagus is necessary to reduce plasma corticosterone when water-restricted rats drink and that the common hepatic vagal branch contributes to the response. These findings implicate the vagus in augmenting rapid removal of circulating corticosterone during relief from stress.

Open-Field Temporal Pattern of Ambulation in Japanese Quail Genetically Selected for Contrasting Adrenocortical Responsiveness to Brief Manual Restraint

Japanese quail selected for a low-stress (LS), rather than a high-stress (HS), plasma corticosterone response to brief restraint have been shown to possess lower fearfulness and a nonspecific reduction in stress responsiveness. Detrended fluctuation analysis provides information on the organization and complexity of temporal patterns of behavior. The present study evaluated the temporal pattern of ambulation of LS and HS quail in an open field that represented a novel environment. Time series of 4,200 data points were collected for each bird by registering the distance ambulated every 0.5 s during a 35-min test period. Consistent with their known reduced fearfulness, the LS quail initiated ambulation significantly sooner (P < 0.02) and tended to ambulate more (P < 0.09) than did their HS counterparts. Detrended fluctuation analyses showed a monofractal series (i.e., a series with similar complexity at different temporal scales) in 72% of the birds. These birds initiated their ambulatory activity in less than 600 s. Among these birds, a lower (P < 0.03) autosimilarity coefficient (α) was found in the LS quail than in their HS counterparts (α = 0.76 ± 0.03 and 0.87 ± 0.03, respectively), suggesting a more complex (less regular) ambulatory pattern in the LS quail. However, when the patterns of ambulation were reexamined by considering only the active period of the time series (i.e., after the birds had initiated their ambulatory activity), monofractal patterns were observed in 97% of the birds, and no differences were found between the lines. Collectively, the results suggest that during the active period of open-field testing, during which fear responses are likely less strong and other motivations are the driving forces of ambulation, the LS and HS lines have similar ambulatory organization.

Influence of Season and Adrenocorticotropic Hormone on Corticosterone in Free-living Female Eastern Fence Lizards (Sceloporus undulatus)

Understanding the proximate mechanism for seasonal modulation of the adrenocortical stress response is an important step in determining the evolutionary significance of such modulation. In vitro studies of adrenocortical cell function in Eastern Fence Lizards (Sceloporus undulatus) have partially explained the mechanism for seasonal changes in male stress responsiveness, but studies of free-living females have not been conducted. Here we test two predictions generated from the in vitro work in free-living female fence lizards: the plasma corticosterone response to adrenocorticotropic hormone injection will be weaker in the postbreeding than the breeding season, and baseline corticosterone levels will be lower in postbreeding than breeding females. Twice during the breeding season and once during the postbreeding season, corticosterone concentrations were measured at capture then again after adrenocorticotropic hormone injection and one hour of confinement. Females robustly responded to adrenocorticotropic hormone, but there was no detectable seasonal difference in the strength of the corticosterone response. Similarly, corticosterone responses did not vary seasonally in females subjected only to confinement without injection. However, as predicted, baseline plasma corticosterone levels were lower in the postbreeding than the breeding season. Plasma triglyceride concentrations varied with season as well as being negatively associated with baseline corticosterone levels. The whole-organism corticosterone response may differ from that of isolated adrenocortical cells which are not subject to either paracrine or upstream hypothalamic and pituitary signals. The mechanism of adrenocortical modulation and its evolutionary significance is most likely to be deciphered by conducting studies at multiple levels of organization.

Antidepressant-like effects of the glucocorticoid receptor antagonist RU-43044 are associated with changes in prefrontal dopamine in mouse models of depression

Chronic corticosterone and isolation rearing paradigms may provide reliable mouse models of depression. Using these models, the present study examined if the specific glucocorticoid receptor antagonist, RU-43044, has an antidepressant-like effect, and studied the possible role of prefrontal neurotransmission on the behavioral effects. Chronic administration of corticosterone and isolation rearing increased the immobility time in the forced swim and tail suspension tests. Subchronic treatment with RU-43044 decreased the immobility time in the forced swim test in chronic corticosterone-treated and isolation-reared mice, but not the control mice. Chronic corticosterone decreased the levels of cortical glucocorticoid receptors and stress-induced increases in plasma corticosterone levels, and blocked the response of plasma corticosterone to dexamethasone, while isolation rearing did not cause any changes in the glucocorticoid receptor system. Both chronic corticosterone and isolation rearing markedly increased high K+-induced dopamine release, but not serotonin release, in the prefrontal cortex. Subchronic RU-43044 reversed the enhanced release of dopamine in the prefrontal cortex of chronic corticosterone-treated and isolation-reared mice. These results suggest that chronic corticosterone and isolation rearing increase the depressive-like behavior in glucocorticoid receptor-dependent and independent manners, respectively, and that RU-43044 shows an antidepressant-like effect, probably via an inhibition of enhanced prefrontal dopaminergic neurotransmission in these mouse models.

Neuroendocrine disorders in adult rats treated prenatally with hydrocortisone acetate

We investigated the effects of hydrocortisone acetate administered to pregnant rats over the last gestational week on some neuroendocrine characteristics in adult female and male offspring. Prenatal glucocorticoid eliminated sex dimorphism of the neurons nuclei volumes in the medial preoptic area and the suprachiasmatic nuclei. There was no elevation of blood plasma corticosterone level after noradrenaline infusion into the third brain ventricle in experimental males; meanwhile, in females adrenocortical response was augmented. Male offspring exhibited a decrease of plasma corticosterone response to an acute stress (1 h restraint) that was not accompanied by post-stress changes neither in the hypothalamic noradrenaline content nor hippocampal glutamate decarboxylase activity. On the contrary, moderate augmentation of adrenocortical stress reactivity and inhibitory effect of GABAergic system were found in females. It was concluded that exposure to prenatal glucocorticoid is able to alter development of the neuroendocrine systems related to reproduction and stress responses both in males and females and resulted in modification of its sex-dimorphic features in adult life.

Influences of Maternal Corticosterone and Selection for Contrasting Adrenocortical Responsiveness in Japanese Quail on Developmental Instability of Female Progeny

Differences in developmental instability were assessed in female offspring of Japanese quail hens selected for reduced (low stress, LS) or exaggerated (high stress, HS) plasma corticosterone (B) response to stress and treated with a placebo or B during egg formation. Hens of each line were implanted (s.c.) with either a silastic tube containing no B (controls) or one filled with B. Female chicks hatched from each of the 4 line × implant treatment combinations were retained for examination of 3 bilateral traits at 130 d of age: length of the tibiotarsus, middle toe length, and distance between the auditory canal and the nares (face length, FL). Greater bilateral trait size variances were associated with measurement of tibiotarsus length (P < 0.04) and middle toe length (P < 0.06) in the HS line, supporting our previous findings in the opposite sex that developmental instability (i.e., fluctuating asymmetry, FA) of certain morphological traits is more pronounced in HS than LS adult quail. The HS quail are also known to exhibit greater adrenocortical responsiveness to a wide range of stressors, and they are more easily frightened than LS birds. Therefore, the line differences in FA (HS > LS) found previously in males and herein in females may simply reflect the differential responsiveness of the birds to chronic social and physical environmental stressors. In addition, the present study detected more (albeit marginally so, P < 0.06) bilateral variability (i.e., heightened FA) in FL of quail hatched from mothers treated with B, a finding entirely due to the very high FL variance observed in the female offspring of B-treated HS hens. Because others have found in ovo B treatment to be associated with heightened FA in chick tarsus bone length and because we have also demonstrated that greater yolk B deposition occurs in eggs from both unstressed and stressed HS quail hens than their LS counterparts, the present maternal B treatment may be acting independently, or in combination with HS genomic effects, to adversely affect developmental stability.

Regulation of resistance against adjuvant arthritis in the Fisher rat.

Inbred female Lewis (LEW/N) rats develop a severe chronic arthritis in the adjuvant arthritis (AA) model, histocompatible Fisher (F344/N) rats are resistant and germ-free Fishers (GF F344) are again susceptible. In this study we show that the F344 rat can become susceptible to AA, using Mycobacterium tuberculosis (M.tb.) in the powerful adjuvant paraffin oil, instead of mineral oil (Freund's incomplete adjuvant (FIA)). This indicates that the F344 rat does not lack T effector cells. To examine further mechanisms responsible for suppression, we determined the level of plasma corticosterone in response to IL-1 alpha in Lewis, F344 and GF F344 rats. IL-1 alpha induced only low amounts of corticosterone in Lewis rats, but high amounts in both F344 and GF F344 rats. The GF F344 rats are susceptible to AA, but the severity of the disease is reduced compared with Lewis rats. This indicates that corticosterone may be an important mechanism to suppress disease development, but not the only mechanism. In addition we investigated whether T suppressor cells play a role in the resistance of the F344 strain. This was performed by pretreating the animals with the immunomodulating drugs cyclophosphamide (Cy) and cyclosporin A (CsA). We were unable to make the F344 rat susceptible to AA, indicating that active suppression does not play a role in the induction phase of arthritis. This finding is confirmed in adoptive transfer experiments of AA from Lewis to F344 rats. Our data suggest the lack of a strong pre-existing suppression in the F344 rats, and indicate that suppression is generated upon bacterial challenge. Whether suppression is overruled probably depends on the power of adjuvants used and potential control by corticosteroids.

The role of the posterior medial bed nucleus of the stria terminalis in modulating hypothalamic–pituitary–adrenocortical axis responsiveness to acute and chronic stress

The bed nucleus of the stria terminalis (BST) plays a prominent role in brain integration of acute responses to stressful stimuli. This study tests the hypothesis that the BST plays a complementary role in regulation of physiological changes associated with chronic stress exposure. Male Sprague-Dawley rats received bilateral ibotenate lesions or sham lesions of the posterior medial region of the BST (BSTpm), an area known to be involved in inhibition of HPA axis responses to acute stress. Chronic stress was induced by 14-day exposure to twice daily stressors in an unpredictable sequence (chronic variable stress, CVS). In the morning after the end of CVS, stressed and non-stressed controls were exposed to a novel restraint stress challenge. As previously documented, CVS caused adrenal hypertrophy, thymic involution, and attenuated body weight gain. None of these endpoints were affected by BSTpm lesions. Chronic stress exposure facilitated plasma corticosterone responses to the novel restraint stress and elevated CRH mRNA. Lesions of the BSTpm increased novel stressor-induced plasma ACTH and corticosterone secretion and enhanced c-fos mRNA induction in the paraventricular nucleus of the hypothalamus (PVN). In addition, lesion of the BSTpm resulted in an additive increase in CVS-induced facilitation of corticosterone responses and PVN CRH expression. Collectively these data confirm that the BSTpm markedly inhibits HPA responses to acute stress, but do not strongly support an additional role for this region in limiting HPA axis responses to chronic drive. The data further suggest that acute versus chronic stress integration are subserved by different brain circuitry.

Non-precocial grey-faced petrel chicks ( Pterodroma macroptera gouldi) show no age-related variation in corticosterone responses to capture and handling

Development patterns in birds range from precocial species, which hatch chicks largely capable of independent existence, to altricial species, chicks of which are highly dependent on their parents for extended periods. Previous work indicates precocial chicks have a robust corticosterone response from hatching whereas non-precocial and altricial chicks have a small response that increases through development. Grey-faced petrels are characteristic of most burrowing procellariiform seabirds with non-precocial chicks that are unable to locomote and are dependent on adults for food, although chicks have well developed downy plumage and can thermoregulate at or soon after hatching. Initial plasma corticosterone concentrations and corticosterone responses to handling were measured during development in semi-precocial grey-faced petrel ( Pterodroma macroptera gouldi) chicks to determine whether they showed a precocial or altricial corticosterone response pattern. Chicks were sampled at six intervals through development from shortly after hatching until close to fledging. Mean corticosterone responses to handling after 30 min were high (115.9 ± 10.7 ng/ml) from 2 to 4 d after hatching and remained high throughout development (70–110 ng/ml). Contrary to expectations for non-precocial chicks, this pattern of corticosterone responses to handling indicates that grey-faced petrel chicks are able to perceive and respond to potential stressors from hatching, a response previously only demonstrated for precocial birds.

Disruption of the CRF2 Receptor Pathway Decreases the Somatic Expression of Opiate Withdrawal

Escape from the extremely aversive opiate withdrawal symptoms powerfully motivates compulsive drug-seeking and drug-taking behaviors. The corticotropin-releasing factor (CRF) system is hypothesized to mediate the motivational properties of drug dependence. CRF signaling is transmitted by two receptor pathways, termed CRF(1) and CRF(2). To investigate the role for the CRF(2) receptor pathway in somatic opiate withdrawal, in the present study we used genetically engineered mice deficient in the CRF(2) receptor (CRF(2)-/-). We employed a novel, clinically relevant mouse model of 'spontaneous' opiate withdrawal as well as a classical opioid receptor antagonist (naloxone)-precipitated opiate withdrawal paradigm. To induce opiate dependence, mice were treated with intermittent escalating morphine doses (20-100 mg/kg, i.p.). We found that 8-128 h after the last opiate injection, CRF(2)-/- mice showed decreased levels of major somatic signs of spontaneous opiate withdrawal, such as paw tremor and wet dog shake, as compared to wild-type mice. Similarly, challenge with naloxone 2 h after the last morphine injection induced lower levels of paw tremor and wet dog shake in CRF(2)-/- mice as compared to wild-type mice. Despite the differences in somatic signs, wild-type and CRF(2)-/- mice displayed similar plasma corticosterone responses to opiate dosing and withdrawal, indicating a marginal role for the hypothalamus-pituitary-adrenal axis in the CRF(2) receptor mediation of opiate withdrawal. Our results unravel a novel role for the CRF(2) receptor pathway in opiate withdrawal. The CRF(2) receptor pathway might be a critical target of therapies aimed at alleviating opiate withdrawal symptoms and reducing relapse to drug intake.

MyD88 signaling in brain endothelial cells is essential for the neuronal activity and glucocorticoid release during systemic inflammation

Activation of neuronal circuits involved in the control of autonomic responses is critical for the host survival to immune threats. The brain vascular system plays a key role in such immune-CNS communication, but the signaling pathway and exact type of cells within the blood-brain barrier (BBB) mediating these functions have yet to be uncovered. To elucidate this issue we used myeloid differentiation factor 88 (MyD88)-deficient mice, because these animals do not show any responses to the cytokine interleukin-1beta (IL-1beta). We created chimeric mice with competent MyD88 signaling in either the BBB endothelium or perivascular microglia of bone marrow origin and challenged them with IL-1beta. Systemic treatment with the cytokine caused a robust transcriptional activation of genes involved in the prostaglandin E(2) (PGE(2)) production by vascular cells of the brain. Upregulation of these genes is dependent on a functional MyD88 signaling in the endothelium, because MyD88-deficient mice that received bone marrow stem cells from wild-type animals (for example, functional perivascular microglia) exhibited no response to systemic IL-1beta administration. MyD88 competent endothelial cells also mediate neuronal activation and plasma release of glucocorticoids, whereas chimeric mice with MyD88-competent perivascular microglia did not show a significant increase of these functions. Moreover, competent endothelial cells for the gene encoding Toll-like receptor 4 (TLR4) are essential for the release of plasma corticosterone in response to low and high doses of lipopolysaccharide. Therefore, BBB endothelial cells and not perivascular microglia are the main target of circulating inflammatory mediators to activate the brain circuits and key autonomic functions during systemic immune challenges.

Long-term habituation to repeated loud noise is impaired by relatively short interstressor intervals in rats.

The phenomenon of spaced (longer intertrial interval) compared with massed (shorter intertrial interval) training leading to better long-term habituation and associative learning is well documented. However, the effects of intertrial intervals on response habituation to repeated stress exposures have not been previously examined. The present experiments found that massed (six 30-min exposures of 95 dB white noise in 6 hr) and spaced (one 30-min exposure daily for 6 days) noise exposures led to similar habituation of plasma corticosterone and ACTH responses, heart rate, and core body temperature after the 6th exposure in male Sprague-Dawley rats. However, these habituated responses were not retained in the massed group on a similar noise re-exposure 48 hr later, compared with the spaced group. The habituated responses found in the massed group after the 6 noise exposures were not due to differential hearing threshold shifts, as examined with modifications of the acoustic startle reflex. These data indicate that relatively short interstressor intervals impair long-term stress adaptation. This series of studies supports the idea of distinct short- and long-term habituation processes to stress responsiveness.

Prenatal dexamethasone exposure affects anxiety-like behaviour and neuroendocrine systems in an age-dependent manner

Prenatal stress has been reported to alter the development of the central nervous system functions. This alteration is thought to be partly caused by increased fetal exposure to glucocorticoid. To clarify how prenatal stress affects neuroendocrine systems and behaviour in an age-dependent manner, we administered a synthetic glucocorticoid, dexamethasone, as a stressor to pregnant rats at gestational days 16–21 and examined the developmental changes in behaviour, hypothalamic corticotropin-releasing factor mRNA expression, corticosterone response and glucocorticoid receptor expression in male offspring. Prenatal dexamethasone exposure decreased corticotropin-releasing factor mRNA in the hypothalamus and disturbed the plasma corticosterone response to restraint stress in the offspring at postnatal week 4 (PW4). In contrast, it was not until PW10 that increased anxiety-like behaviour emerged in the dexamethasone-exposed offspring. In association with the acquisition of increased anxiety-like behaviour at PW10, glucocorticoid receptor expression was decreased in the amygdala in dexamethasone-exposed offspring at PW7 and PW10. Thus, our longitudinal analysis suggests that prenatal exposure to glucocorticoid hampers neuroendocrinological development in the offspring during early life, and that this disturbance results in the induction of increased anxiety-like behaviour in adulthood.

The Anteroventral Bed Nucleus of the Stria Terminalis Differentially Regulates Hypothalamic-Pituitary-Adrenocortical Axis Responses to Acute and Chronic Stress

The anteroventral region of the bed nucleus of the stria terminalis (BST) stimulates hypothalamic-pituitary-adrenocortical (HPA) axis responses to acute stress. However, the role of the anterior BST nuclei in chronic drive of the HPA axis has yet to be established. Therefore, this study tests the role of the anteroventral BST in physiological responses to chronic drive, using a chronic variable stress (CVS) model. Male Sprague-Dawley rats received either bilateral ibotenate lesions, targeting the anteroventral BST, or vehicle injection into the same region. Half of the lesion and control rats were exposed to a 14-d CVS paradigm consisting of twice-daily exposure to unpredictable, alternating stressors. The remaining rats were nonhandled control animals that remained in home cages. On the morning after the end of CVS exposure, all rats were exposed to a novel restraint stress challenge. CVS induced attenuated body weight gain, adrenal hypertrophy, thymic involution, and enhanced CRH mRNA in hypophysiotrophic neurons of the hypothalamic paraventricular nucleus, none of which were affected by anteroventral BST lesions. In the absence of CVS, lesions attenuated the plasma corticosterone and paraventricular nucleus c-fos mRNA responses to the acute restraint stress. In contrast, lesions of the anteroventral BST elevated plasma ACTH and corticosterone responses to novel restraint in the rats previously exposed to CVS. These data suggest that the anterior BST plays very different roles in integrating acute stimulation and chronic drive of the HPA axis, perhaps mediated by chronic stress-induced recruitment of distinct BST cell groups or functional reorganization of stress-integrative circuits.

Ontogeny of the Cloacal Gland in Male Japanese Quail Classified in a T-Maze

Broiler chicks that traverse a T-maze quickly to reinstate contact with their companions (HP, high performers) are known to grow faster, are more social, and have a reduced plasma corticosterone response to acute stress than slower chicks (LP, low performers). High-performing quail from a line selected for reduced rather than exaggerated (high-stress) adrenocortical stress responsiveness also show enhanced female reproductive performance when compared with LP–high-stress quail. Herein, time courses of male sexual development were evaluated in genetically unremarkable quail that were categorized at 2 d of age as HP or LP in the T-maze. Body weight, cloacal gland volume (CVOL), proportion of individuals that produced cloacal gland foam, intensity of foam production, and CVOL relative to BW (RCVOL) were determined weekly from 4 to 10 wk of age, and again at 22 wk, along with absolute and BW-adjusted testes weight. Although CVOL and RCVOL were initially similar in both T-maze groups, both variables were greater (P < 0.05) in HP than in LP quail between 6 and 10 wk of age. High-performing birds also showed a trend (P < 0.1) of greater cloacal gland foam than their LP counterparts from 5 to 7 wk. From 8 wk on, all birds were in foam production. Intensity of foam production results generally mimicked those found for CVOL and RCVOL. Body weights were higher (P < 0.05) in HP than LP quail from 5 to 7 wk. No T-maze group differences were found in any of the variables at 22 wk of age. The results suggest that rapid negotiation of the T-maze is associated with accelerated growth and puberty in male quail, although the enhanced reproductive development of HP males does not remain extant in aged adults.

Corticosterone and time–activity budget: An experiment with Black-legged kittiwakes

In vertebrates, the well established increase in plasma corticosterone in response to food shortage is thought to mediate adjustments of foraging behavior and energy allocation to environmental conditions. However, investigating the functional role of corticosterone is often constrained by the difficulty to track time–activity budget of free-ranging animals. To examine how an experimental increase in corticosterone affects the activity budget of male Black-legged kittiwakes ( Rissa tridactyla), we used miniaturized activity loggers to record flying/foraging, presence on the sea surface and nest attendance. To investigate how corticosterone affects allocation processes between self-foraging and foraging devoted to the brood, we monitored body mass change of males from capture (day 0) to recapture (day 3). Among control birds, males in poor condition at day 0 spent significantly more time flying/foraging and less time attending the nest site than did males in good condition. Corticosterone treatment affected time spent flying/foraging in interaction with body condition at day 0: corticosterone-implanted males in good condition spent more time flying/foraging than control ones; this was not observed in poor condition males. In control birds, change in body mass was negatively correlated with body condition at day 0. This was reinforced by corticosterone treatment and, on average, corticosterone-implanted males gained much more mass than controls. These results suggest that in Black-legged kittiwakes, body condition and corticosterone levels can interact to mediate foraging decisions and possibly energy allocation: when facing stressful environmental conditions, birds in good body condition may afford to increase the time spent foraging probably to maintain brood provisioning, whereas poor body condition birds seemed rather to redirect available energy from reproduction to self-maintenance.