Increase In Plasma Corticosterone Concentration Research Articles

Paraventricular nucleus modulates autonomic and neuroendocrine responses to acute restraint stress in rats

The paraventricular nucleus of the hypothalamus (PVN) has been implicated in several aspects of neuroendocrine and cardiovascular control. The PVN contains parvocellular neurons that release the corticotrophin release hormone (CRH) under stress situations. In addition, this brain area is connected to several limbic structures implicated in defensive behavioral control, as well to forebrain and brainstem structures involved in cardiovascular control. Acute restraint is an unavoidable stress situation that evokes corticosterone release as well as marked autonomic changes, the latter characterized by elevated mean arterial pressure (MAP), intense heart rate (HR) increases and decrease in the tail temperature. We report the effect of PVN inhibition on MAP and HR responses, corticosterone plasma levels and tail temperature response during acute restraint in rats. Bilateral microinjection of the nonspecific synaptic blocker CoCl 2 (1 mM/100 nL) into the PVN reduced the pressor response; it inhibited the increase in plasma corticosterone concentration as well as the fall in tail temperature associated with acute restraint stress. Moreover, bilateral microinjection of CoCl 2 into areas surrounding the PVN did not affect the blood pressure, hormonal and tail vasoconstriction responses to restraint stress. The present results show that a local PVN neurotransmission is involved in the neural pathway that controls autonomic and neuroendocrine responses, which are associated with the exposure to acute restraint stress.

Pharmacodynamic and Pharmacokinetic Characterization of the Aldosterone Synthase Inhibitor FAD286 in Two Rodent Models of Hyperaldosteronism: Comparison with the 11β-Hydroxylase Inhibitor Metyrapone

Aldosterone synthase (CYP11B2) inhibitors (ASIs) represent an attractive therapeutic approach for mitigating the untoward effects of aldosterone. We characterized the pharmacokinetic/pharmacodynamic relationships of a prototypical ASI, (+)-(5R)-4-(5,6,7,8-tetrahydroimidazo[1,5-a]pyridin-5-yl]benzonitrile hydrochloride (CGS020286A, FAD286, FAD) and compared these profiles to those of the 11beta-hydroxylase inhibitor metyrapone (MET) in two rodent models of secondary hyperaldosteronism and corticosteronism. In chronically cannulated Sprague-Dawley rats, angiotensin II (ANG II) (300 ng/kg bolus + 100 ng/kg/min infusion) or adrenocorticotropin (100 ng/kg + 30 ng/kg/min) acutely elevated plasma aldosterone concentration (PAC) from approximately 0.26 nM to a sustained level of approximately 2.5 nM for 9 h. Adrenocorticotropin but not ANG II elicited a sustained increase in plasma corticosterone concentration (PCC) from approximately 300 to approximately 1340 nM. After 1 h of Ang II or adrenocorticotropin infusion, FAD (0.01-100 mg/kg p.o.) or MET (0.1-300 mg/kg p.o.) dose- and drug plasma concentration-dependently reduced the elevated PACs over the ensuing 8 h. FAD was approximately 12 times more dose-potent than MET in reducing PAC but of similar or slightly greater potency on a plasma drug concentration basis. Both agents also decreased PCC in the adrenocorticotropin model at relatively higher doses and with similar dose potencies, whereas FAD was 6-fold weaker based on drug exposures. FAD was approximately 50-fold selective for reducing PAC versus PCC, whereas MET was only approximately 3-fold selective. We conclude that FAD is a potent, orally active, and relatively selective ASI in two rat models of hyperaldosteronism. MET is an order of magnitude less selective than FAD but is, nevertheless, more potent as an ASI than as an 11beta-hydroxylase inhibitor.

Lowering Effects of Allyl Isothiocyanate on the Number of Lymphocyte and Its Subsets in Rats

The purpose of this study was to elucidate the effects of a main pungent component of wasabi, allyl isothiocyanate (AITC), on the number of lymphocytes, T-lymphocyte, B-lymphocyte and natural killer (NK) cells and plasma corticosterone concentrations in rats. AITC was given as either single dosage [20 mg/kg body weight per day; subcutaneous (s.c.) and oral] or as a daily dosage (10 mg and 20 mg/kg body weight per day; s.c.) for 4 days for the hourly and daily assessment of changes in the numbers of lymphocytes, respectively. A single s.c. injection or oral administration of AITC significantly reduced the number of lymphocytes at 4 hr to approximately 0.68 times, indicating that decreased effects of AITC on the number of lymphocytes are independent on the administration route. Administration of AITC for 4 days reduced dose-dependently the number of lymphocytes, and significantly reduced the number of T-lymphocyte and B-lymphocyte to 0.79 and 0.60 times, respectively. However, the number of NK cells did not change by AITC. Administration of AITC increased plasma corticosterone concentrations at 4 day of post s.c. injection to 5.4-6.0 times. These results suggest that AITC-mediated immunosuppresion is at least in part attributable to changes in the number and distribution of lymphocyte and its subsets.

Long-term postpartum anxiety and depression-like behavior in mother rats subjected to maternal separation are ameliorated by palatable high fat diet

While the effects of maternal separation on pups are well studied, the impact on dams has attracted little attention. The consumption of palatable food is known to dampen stress responses in animals, and emotions influence food choice in humans. Here we examined the early- and long-term impacts of maternal separation on behavioral profile of the dams, and the effects of palatable cafeteria high-fat diet (HFD). After littering, Sprague–Dawley female rats were subjected to prolonged separation, S180 (180min) or brief separation, S15 (15min/day) from postnatal days (PND) 2–14. At 4 weeks postpartum, half the dams were assigned to HFD. Anxiety and depression-like behaviors were assessed pre- and post-diet. Compared to S15 dams, S180 dams consuming chow demonstrated increased anxiety and depression-like behaviors assessed by elevated plus maze (EPM) and forced swim (FST) tests, respectively. These behavioral deficits were observed at 4 weeks, and persisted until 17 weeks postpartum. The S180 dams also had increased plasma corticosterone concentration compared to S15 dams, which coincided with increased hypothalamic CRH mRNA and reduced hippocampal GR mRNA expression, suggesting possible dysregulation of hypothalamic-pituitary-adrenal axis activity. Interestingly, continuous provision of HFD improved the behavioral deficits observed in S180 dams with significant reduction of hypothalamic CRH mRNA expression. These data are the first to describe long-term detrimental behavioral impacts of separation in dams, suggesting this may provide a model of postpartum depression. Moreover, they support the notion of long-term beneficial effects of ‘comfort food’ on stress responses.

Reduced emotional and corticosterone responses to stress in μ-opioid receptor knockout mice

The detailed mechanisms of emotional modulation in the nervous system by opioids remain to be elucidated, although the opioid system is well known to play important roles in the mechanisms of analgesia and drug dependence. In the present study, we conducted behavioral tests of anxiety and depression and measured corticosterone concentrations in both male and female μ-opioid receptor knockout (MOP-KO) mice to reveal the involvement of μ-opioid receptors in stress-induced emotional responses. MOP-KO mice entered more and spent more time in the open arms of the elevated plus maze compared with wild-type mice. MOP-KO mice also displayed significantly decreased immobility in a 15 min tail-suspension test compared with wild-type mice. Similarly, MOP-KO mice exhibited significantly decreased immobility on days 2, 3, and 4 in a 6 min forced swim test conducted for 5 consecutive days. The increase in plasma corticosterone concentration induced by tail-suspension, repeated forced swim, or restraint stress was reduced in MOP-KO mice compared with wild-type mice. Corticosterone levels were not different between wild-type and MOP-KO mice before stress exposure. In contrast, although female mice tended to exhibit fewer anxiety-like responses in the tail-suspension test in both genotypes, no significant gender differences were observed in stress-induced emotional responses. These results suggest that MOPs play an important facilitatory role in emotional responses to stress, including anxiety- and depression-like behavior and corticosterone levels.

Cadmium exposure during pregnancy reduces birth weight and increases maternal and foetal glucocorticoids

Cadmium exposure induces low birth weight through unknown mechanisms. Since low birth weight is associated to foetal exposure to high glucocorticoids (GC) concentrations, we hypothesized that low birth weight induced by prenatal exposure to Cd(2+) is, at least in part, mediated by higher foetal exposure to GC, specifically corticosterone, the main active GC in rodents. Pregnant rats were exposed to different dose of CdCl(2) administered in drinking water during the whole pregnancy period. At term, corticosterone was measured by enzyme immunoassay in maternal and foetal blood and in placental tissues. Cadmium was determined in placentas, maternal tissues (liver and kidney) and foetuses by inductively coupled plasma-mass spectrometry (ICP-MS). Placental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) activity and expression were determined by a radiometric conversion assay and quantitative RT-PCR respectively. Results demonstrated that 50 ppm of Cd(2+), which was accumulated in different maternal tissues but not in the foetus, reduced pup birth weights and increased plasma corticosterone concentrations, both in mother and foetus. Placental 11beta-HSD2 activity and expression did not change by the treatment. We conclude that 50 ppm of Cd(2+) administered during pregnancy, increase foetal corticosterone concentrations due, probably, to alterations of the regulatory mechanisms of placental barrier to GC causing a mild but significant reduced birth weight.

Satiety induced by central stresscopin is mediated by corticotrophin-releasing factor receptors and hypothalamic changes in chicks

The central mechanism that mediates stresscopin (SCP)-induced satiety is poorly understood, and its effect on avian appetite is not documented. Thus, this study was conducted to elucidate some of the central and behavioral mechanisms that are associated with SCP-induced satiety using broiler- and layer-type chicks ( Gallus gallus) as model organisms. In Experiment 1, broiler-type chicks responded with decreased food and water intake but had increased plasma corticosterone concentration after intracerebroventricular (ICV) SCP injection. However, the effect on water intake was secondary to food intake, since food-restricted SCP-treated broiler-type chicks did not reduce water intake in Experiment 2. In Experiment 3, layer-type chicks responded with decreased food intake at much lower doses than broiler-type chicks. In Experiment 4, astressin (a non-selective corticotrophin-releasing factor [CRF] receptor antagonist) prevented SCP-induced anorexia in broiler-type chicks. In Experiment 5, SCP-treated broiler-type chicks had an increased number of c-Fos immunoreactive cells in the ventromedial hypothalamus, parvicelluar and magnocellular divisions of the paraventricular nucleus and the periventricular nucleus. In Experiment 6, SCP-treated broiler-type chicks had decreased feeding pecks and increased jumping, distance moved and more escape attempts. Thus, we conclude that central SCP causes anorexigenic and other behavioral effects in chicks, and the hypothalamus and CRF receptors are involved.

Lactation modifies stress-induced immune changes in laboratory rats

Lactation and stressor exposure both influence the activity of the immune system, but the interaction of both factors on the immune defense is poorly understood. The aim was therefore to investigate in lactating Long–Evans rats the effect of social stress on aspects of cellular immunity in the blood and mesenteric lymph nodes (MLN). Acute social stress (2 h) was induced in lactating and non-lactating female intruders using a confrontation model that yielded into social defeat and increased plasma corticosterone concentrations. Stress as well as lactation had marked effects on the immune system. Acute social stress caused granulocytosis, reduced lymphocyte proliferation, and cytokine production in the blood, but had no significant effects in MLN. In the blood of lactating rats, increased numbers of granulocytes and enhanced phagocytosis, but decreased B cell numbers and reduced IL-2 production was observed. However, in MLN both lymphocyte proliferation and monocyte numbers were increased in lactating rats. The effect of stress on the immune measures was often similar in lactating and non-lactating females, but a few important differences were evident: Only non-lactating animals showed an increase in blood granulocyte numbers and a decrease in IL-2 production in response to stressor exposure. Thus, during lactation, a neuroendocrine status may exist which impedes stress-induced modulations at least of some immune parameters.

Exposure to pheromones increases plasma corticosterone concentrations in a terrestrial salamander

Sensory cues involved in social interactions can influence plasma steroid hormone concentrations. Although pheromonal communication is common in amphibians, it is unknown whether pheromones can alter hormone levels in amphibians as they do in mammals. We tested whether courtship pheromones would alter steroid hormone concentrations in male and female terrestrial salamanders ( Plethodon shermani). Plasma corticosterone concentrations were elevated in male salamanders exposed to mental gland courtship pheromones, as compared to males exposed to female skin secretions or a saline control. Chemosensory cues had no effect on testosterone levels in males or on corticosterone or estradiol levels in females. These results provide the first evidence that pheromones have priming effects on the endocrine system in amphibians.

Fluoxetine inhibits corticotropin-releasing factor (CRF)-induced behavioural responses in rats

Corticotropin-releasing factor (CRF) is a potent neuromodulator of stress-related behaviour but the neural mechanisms underlying these effects are not clear. Studies were designed to test the hypothesis that CRF-induced behavioural arousal involves interactions with brainstem serotonergic systems. To examine interactions between CRF and serotonergic systems in the regulation of behaviour, CRF (1 μg, intracerebroventricular (i.c.v.)) or vehicle was infused in the presence or absence of the selective serotonin re-uptake inhibitor fluoxetine (0, 0.1, 1 or 10 mg/kg, intravenous (i.v.)). Fluoxetine was used at these doses because it is known to decrease serotonin cell firing rates while increasing extracellular serotonin concentrations in select forebrain regions. We then measured behavioural, neurochemical and endocrine responses. CRF increased locomotion and spontaneous non-ambulatory motor activity (SNAMA) in the home cages. Fluoxetine decreased tissue 5-hydroxyindoleacetic acid concentrations, a measure of serotonin metabolism, in specific limbic brain regions of CRF-treated rats (nucleus accumbens shell region, entorhinal cortex, central nucleus of the amygdala). Furthermore, fluoxetine inhibited CRF-induced SNAMA. CRF and fluoxetine independently increased plasma corticosterone concentrations, but the responses had distinct temporal profiles. Overall, these data are consistent with the hypothesis that CRF-induced facilitation of behavioural activity is dependent on brainstem serotonergic systems. Therefore, fluoxetine may attenuate or alleviate some behavioural responses to stress by interfering with CRF-induced responses.

Effect of calcitonin gene-related peptide (CGRP) on avian appetite-related processes

Calcitonin gene-related peptide (CGRP) is released from the gastrointestinal tract following ingestion and causes satiety in mammals. Its effects on appetite in non-mammalian vertebrates are unreported. In Experiment 1, fasted chicks reduced food and water intake after central injection of CGRP. These effects were not associated with increased plasma corticosterone concentration. In Experiment 2, we showed that the effect on water intake was independent of food intake. In Experiment 3, central CGRP caused increased c-Fos immunoreactivity in the arcuate (ARC) nucleus, paraventricular nucleus (PVN), periventricular (PHN) and ventromedial (VMH) hypothalamic nuclei. The results of Experiment 4 demonstrate that intraperitoneal injection of CGRP also causes reduced food and water intake. c-Fos immunoreactivity was increased in the ARC, PHN, PVN and VMH in Experiment 5 after intraperitoneal injection of CGRP. Lastly in Experiment 6, we showed that central CGRP changes the type of pecks from feeding to exploratory, and reduces the number of escape attempts. The effect of CGRP appears to be primary on appetite in chicks. In conclusion, the mechanisms of CGRP induced satiety have some similarities and differences between avian and rodent models. The results presented here provide new insight into the evolution of vertebrate satiety regulatory mechanisms.

Determination of corticosterone concentrations in egg albumen: A non-invasive indicator of stress in laying hens

Measurement of plasma corticosterone is difficult because the handling associated with blood sampling from birds is stressful. The use of non-invasive means of measuring stress could help to alleviate this problem. It was considered that the accumulation of plasma corticosterone into the egg albumen could provide a non-invasive indicator of stress in laying hens. The present study examined the relationship between plasma and egg albumen corticosterone concentrations and then determined what affect exposing hens to known stressors had on egg albumen corticosterone concentrations. Laying hens were given subcutaneous injections of either 0, 5, or 10 mg of corticosterone suspended in peanut oil and then the concentrations of corticosterone in the plasma and egg albumen determined. Also, groups of hens were handled, exposed to high ambient temperature and moved to new cages, all events known to be stress provoking, and then the concentrations of corticosterone in albumen determined. The injections increased plasma corticosterone concentrations substantially and these were directly related to the concentrations measured in the egg albumen. When hens were exposed to the various stressors, the level of corticosterone in the egg albumen increased. The corticosterone concentrations found in the egg albumen can provide a convenient non-invasive means of measuring stress in laying hens and other birds.

Post-adrenalectomy changes in the gene expression of specific G-protein subunits involved in morphine sensitization

There are some reports indicating that adrenalectomy significantly potentiates morphine-induced analgesia. Since G-protein subunits have an important role in morphine effects at the cellular level and the exact mechanism(s) of adrenalectomy-induced morphine sensitization has not yet been clarified, the present study was designed to determine the changes in the levels of Galphai/o, Galphas, Gbeta mRNA involved in this phenomenon. All experiments were carried out on male Wistar rats. The tail-flick test was used to assess the nociceptive threshold and corticosterone levels were measured by radioimmunoassay as a marker of HPA function. The dorsal half of the lumbar spinal cord was assayed for the expression of G-protein subunits using semiquantitative PCR normalized to beta-actin gene expression. Results showed that morphine not only in 3 mg/kg, but also in a sub-effective dose (2 mg/kg) could affect the nociceptive threshold and induce an analgesic response in adrenalectomized (ADX) rats while 2 mg/kg morphine did not demonstrate analgesic properties in sham-operated animals. These effects were reversed with corticosterone replacement. Morphine increased plasma corticosterone concentration in a dose-dependent manner in sham-operated rats. Following adrenalectomy a significant increase in the mRNA levels of Galphai/o (79%) and Gbeta (96%) was observed in the dorsal portion of the lumbar spinal cord. In contrast, no significant changes were observed in the mRNA level of Galphas. In conclusion, our results demonstrate that the levels of the cellular components involved in morphine analgesia significantly increase in ADX animals. This may be at least partly responsible for adrenalectomy-induced morphine sensitization.

β‐Melanocyte‐Stimulating Hormone Potently Reduces Appetite Via the Hypothalamus in Chicks

The melanocortin system together with other appetite-related systems plays a significant role in appetite regulation. The appetite-related effects of one such melanocortin, beta-melanocyte-stimulating hormone (MSH), are well documented in rodents; however, its effects in the avian class are not thoroughly understood. Thus, we designed a study to determine the effects of i.c.v. beta-MSH injection on food and water intake, plasma corticosterone concentration, ingestive and non-ingestive behaviours, and hypothalamic neuronal activation using Cobb-500 chicks. Chicks responded to beta-MSH-treatment with a reduction in food and water intake; however when water intake was measured independently of food intake, it was not affected. beta-MSH-treated chicks also had increased plasma corticosterone concentrations and increased c-Fos reactivity in the periventricular, paraventricular and infundibular nuclei, and the ventromedial hypothalamus; however, the lateral hypothalamus was not affected. The effect on food intake is primary because behaviours that may be competitive with food intake were not increased in beta-MSH-treated chicks. Based on these results, we conclude that beta-MSH causes anorexigenic effects that are likely primarily mediated via stimulation of satiety-related hypothalamic nuclei in broiler-type chicks.

Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats

Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTH-secreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an approximately 70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance.

Effects of chronic social stress in adolescence on anxiety and neuroendocrine response to mild stress in male and female rats

Using a rat model of adolescent social stress (SS, daily 1 h isolation and change of cage partner, 30–45 days of age), we have reported sex-specific effects on neuroendocrine function over the course of SS, and enduring effects of SS in females, and not males, on drug-related behaviour. Here, we investigated both the immediate and enduring impact of SS in adolescence on anxiety-like behaviour in the elevated plus maze (EPM) and determined the temporal pattern of corticosterone release after confinement to the open arm of the EPM. When tested as adolescents, SS decreased anxiety-like behaviour in females and had no effect in males. When tested as adults several weeks after the chronic stress, overall, SS tended to increase anxiety-like behaviour in both sexes. However, estrous cycle moderated the effect in females, in that reduced anxiety-like behaviour was observed for SS females in the estrous group. Confinement to the open arm of the EPM increased plasma corticosterone concentrations, which declined markedly upon return to home cage for all except adolescent control males for which corticosterone concentrations at 45 and 90 min were elevated compared other groups. Among controls, anxiety-like behaviour decreased in females and increased in males with age, and confinement to the open arm of the EPM led to a greater increase in corticosterone concentrations in adult males compared to adolescent males. In sum, modest effects of adolescent social stress were observable several weeks after the stress exposure, indicating that sex-specific developmental trajectories and vulnerability to anxiety may be shaped by experiences in adolescence.

Amylin causes anorexigenic effects via the hypothalamus and brain stem in chicks

This study was conducted to determine the effects of amylin on appetite-related processes in chicks. Broiler chicks were centrally and peripherally injected with amylin, and feed and water intake were quantified. Feed intake was reduced after both central and peripheral amylin, but water intake was not affected. To determine if the hypothalamus and brainstem were involved in the anorexigenic effect, chicks were centrally and peripherally injected with amylin, and c-Fos immunoreactivity was quantified in the lateral hypothalamus (LH), ventromedial hypothalamus (VMH), area postrema (AP) and the nucleus of the solitary tract (NTS). Amylin decreased c-Fos immunoreactivity in the LH, did not affect the VMH, and increased c-Fos immunoreactivity in the AP and NTS. To determine if alimentary transit time was affected, chicks received central amylin and were gavaged with chicken feed slurry containing a visible marker. Amylin-treated chicks had increased alimentary canal transit time. Chicks also responded to central amylin with increased anxiety-related behaviors and increased plasma corticosterone concentration. These results demonstrate that amylin affects feeding, alimentary canal transit, and behavior through hypothalamic and brainstem mechanisms in chicks.

Distinct behavioral and neurochemical alterations induced by intermittent hypoxia or paradoxical sleep deprivation in rats

The current study investigated the effects of paradoxical sleep deprivation and intermittent hypoxia by examining whether a combination of the two would induce anxiety-like alterations in behavior. The neurochemical effects of these manipulations were investigated by measuring cortical, striatal and hippocampal monoamine concentrations. Wistar Hannover rats were submitted to subchronic (3 days) intermittent hypoxia exposure (alternating cycles of 2 min room air–2 min 10% O 2 from 0700–1900 h) and paradoxical sleep deprivation using the single platform method. Rats were randomly assigned to four different protocols: 1) control, 2) intermittent hypoxia during the light period (12 h/day), 3) paradoxical sleep deprivation (24 h/day), and 4) intermittent hypoxia combined with paradoxical sleep deprivation. Rats subjected to intermittent hypoxia showed no modification in the behavioral or neurochemical parameters assessed. Although paradoxical sleep deprivation did not produce alterations in anxiety-like behavior, the rats did increase exploratory activity in the elevated plus-maze. Moreover, a significant increase in striatal epinephrine and hippocampal homovanilic acid (HVA) concentrations was found in the paradoxical sleep deprivation groups, but not in the intermittent hypoxia/paradoxical sleep deprivation group. Of note, both paradoxical sleep deprivation and intermittent hypoxia/paradoxical sleep deprivation groups showed an increase in plasma corticosterone concentration. These results suggest that paradoxical sleep deprivation induces behavioral alterations, and these abnormalities may reflect altered neurotransmission in the brain. When paradoxical sleep deprivation was combined with intermittent oxygen depletion, the behavioral and biochemical parameters were comparable to those of control rats.

Prenatal undernutrition decreases the sensitivity of the hypothalamo-pituitary-adrenal axis in rat, as revealed by subcutaneous and intra-paraventricular dexamethasone challenges

Prenatal undernutrition is known to disturb the hypothalamo-pituitary-adrenal (HPA) axis, possibly through the programming of decreased expression of hypothalamic and pituitary glucocorticoid receptors. To test this hypothesis, we examined the corticosterone response to moderate subcutaneous (100 μg/kg) and intra-paraventricular (50 pmol, bilaterally) dexamethasone (DEX) challenges in normal eutrophic and prenatally undernourished young rats. Undernutrition was induced during fetal life by restricting the diet of pregnant mothers to 10 g daily, while mothers of eutrophic rats received the same diet ad libitum. At day 40 of postnatal life (i) undernourished rats showed increased plasma corticosterone concentration compared to normals; and (ii) subcutaneous and intra-paraventricular administrations of DEX led to reduced corticosterone levels in normal and undernourished animals, the effect of DEX (administered either peripherally or centrally) being significantly lower in the latter group. Results suggest that the low sensitivity of the HPA axis to DEX as well as the increased plasma corticosterone observed in prenatally undernourished rats could be due to the already reported glucocorticoid receptor underexpression found in the hypothalamus and pituitary of in utero undernourished animals, but alternative explanations involving central noradrenergic adaptive changes could also be possible.

Corticosterone in relation to body mass in Adelie penguins ( Pygoscelis adeliae) affected by unusual sea ice conditions at Ross Island, Antarctica

Penguins naturally fast each year during breeding and again whilst moulting, and may lose more than 40% of body mass during a fast. Fasting in emperor ( Aptenodytes forsteri) and king ( Aptenodytes patagonicus) penguins has been divided into three phases, with phase III characterised by an increased rate of body mass loss, increased plasma corticosterone concentrations, and a change in behaviour leading to abandonment of the breeding attempt and return to sea to feed. Initial corticosterone concentrations and corticosterone responses to a handling stressor were measured in the current study to determine if they increase during phase III of fasting in Adelie penguins ( Pygoscelis adeliae). The study was conducted in 2001 at the northern Cape Bird colony on Ross Island, Antarctica. Penguin breeding on Ross Island was disrupted in the 2001–2002 summer by a large iceberg (B15A) which stopped the normal movement of sea ice in the Ross Sea. Penguins departing from the Cape Bird colony were lighter than returning or incubating birds (3.39 ± 0.10 cf. 4.16 ± 0.06 and 4.07 ± 0.08 kg). It is likely that the departing birds were males that had been lighter than normal when they arrived at the colony. Initial plasma corticosterone concentrations were higher in departing than returning or incubating penguins (6.89 ± 1.69 cf. 2.36 ± 0.42 and 1.08 ± 0.19 ng/ml). Corticosterone responses to handling were also greater in departing penguins. Initial plasma corticosterone, concentrations at 30 min and total and corrected integrated corticosterone responses were inversely related to body mass in departing penguins, whereas there were no relationships in arriving penguins. β-hydroxybutyrate and uric acid concentrations were consistent with departing birds having entered phase III of fasting. The results indicate that corticosterone and corticosterone responses are elevated in phase III of fasting in the Adelie penguin.