scholarly journals The Effect of Neonatal Maternal Stress on Plasma Levels of Adrenocorticotropic Hormone, Corticosterone, Leptin, and Ghrelin in Adult Male Rats Exposed to Acute Heterotypic Stressor

2016 ◽  
pp. S557-S566 ◽  
Author(s):  
A. HOLUBOVÁ ◽  
A. ŠTOFKOVÁ ◽  
J. JURČOVIČOVÁ ◽  
R. ŠLAMBEROVÁ
Keyword(s):  
Hpa Axis ◽  
Adult Male ◽  
Plasma Levels ◽  
Adrenocorticotropic Hormone ◽  
Acute Stress ◽  
Male Rats ◽  
Lower Sensitivity ◽  
Male Progeny ◽  
Swimming Stress ◽  
Plasma Leptin

Activation of the hypothalamic-pituitary-adrenal (HPA) axis is important for maintenance of homeostasis during stress. Recent studies have shown a connection between the HPA axis and adipose tissue. The present study investigated the effect of acute heterotypic stress on plasma levels of adrenocorticotropic hormone (ACTH), corticosterone (CORT), leptin, and ghrelin in adult male rats with respect to neonatal maternal social and physical stressors. Thirty rat mothers and sixty of their male progeny were used. Pups were divided into three groups: unstressed control (C), stressed by maternal social stressor (S), stressed by maternal social and physical stressors (SW). Levels of hormones were measured in adult male progeny following an acute swimming stress (10 min) or no stress. ELISA immunoassay was used to measured hormones. The ACTH and CORT levels were significantly increased in all groups of adult progeny after acute stress; however, CORT levels were significantly lower in both neonatally stressed groups compared to controls. After acute stress, plasma leptin levels were decreased in the C and SW groups but increased in the S group. The data suggest that long-term neonatal stressors lead to lower sensitivity of ACTH receptors in the adrenal cortex, which could be a sign of stress adaptation in adulthood. Acute stress in adult male rats changes plasma levels of leptin differently relative to social or physical neonatal stressors.

Insulin sensitivity, leptin, adiponectin, resistin, and testosterone in adult male and female rats after maternal-neonatal separation and environmental stress

2018 ◽  
Vol 314 (1) ◽  
pp. R12-R21 ◽  
Author(s):  
Hershel Raff ◽  
Brian Hoeynck ◽  
Mack Jablonski ◽  
Cole Leonovicz ◽  
Jonathan M. Phillips ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adult Male ◽  
Rat Model ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Neonatal Hypoxia ◽  
Male And Female Rats ◽  
Plasma Leptin ◽  
Neonatal Separation

Care of premature infants often requires parental and caregiver separation, particularly during hypoxic and hypothermic episodes. We have established a neonatal rat model of human prematurity involving maternal-neonatal separation and hypoxia with spontaneous hypothermia prevented by external heat. Adults previously exposed to these neonatal stressors show a sex difference in the insulin and glucose response to arginine stimulation suggesting a state of insulin resistance. The current study used this cohort of adult rats to evaluate insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and testosterone. The major findings were that daily maternal-neonatal separation led to an increase in body weight and HOMA-IR in adult male and female rats and increased plasma leptin in adult male rats only; neither prior neonatal hypoxia (without or with body temperature control) nor neonatal hypothermia altered subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; male-female differences in resistin were lost in the adults that were exposed to hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone in adult male rats. We conclude that neonatal stressors result in subsequent adult sex-dependent increases in insulin resistance and adipokines and that our rat model of prematurity with hypoxia without hypothermia alters adult testosterone dynamics.

Neonatal hyperthyroidism: effects on sympathetic responses to stress in adult rats

1983 ◽  
Vol 245 (1) ◽  
pp. R95-R99
Author(s):  
R. McCarty ◽  
R. F. Kirby ◽  
P. C. Brunjes
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Acute Stress ◽  
Male Rats ◽  
Adult Rats ◽  
Basal Plasma ◽  
Repeated Sampling ◽  
Neonatal Hyperthyroidism ◽  
Sympathetic Nervous

Treatment of developing rats with thyroid hormone results in accelerated maturation of sympathetic and adrenal medullary responses to reflex activation of central sympathetic outflow. In this study, we examined the effects of neonatal hyperthyroidism on the responsiveness of the sympathetic nervous system of adult rats to acute stress. Hyperthyroidism was produced in Long-Evans hooded rats by injections of thyroxine (neo-T4, 1 mg/kg body wt) on postnatal days 1-4. Littermate controls received injections of vehicle only. In adulthood, male rats of the two groups were prepared with chronic tail artery catheters to allow repeated sampling of blood and direct measurements of mean arterial pressure (MAP, mmHg) and heart rate (HR, beats/min). Two days after surgery, rats were stressed by exposure to 1 min of inescapable foot shock (2.0 mA, 0.6-s duration, every 6 s). The activity of the sympathetic nervous system was assessed by measuring plasma levels of norepinephrine (NE) and epinephrine (E). Basal plasma levels of NE and E and resting MAP did not differ between neo-T4 and control rats. However, basal HR was elevated in neo-T4 rats. Footshock-induced increments in plasma levels of both catecholamines were greater in neo-T4 compared with control rats even though behavioral responses to footshock were similar across groups. However, neo-T4 rats were more active when tested in an open field on each of 3 consecutive days. These findings indicate that neonatal treatment with T4 results in hyperresponsiveness of the sympathoadrenal medullary system to acute stress that persists into adulthood.

scholarly journals Facilitation of the HPA Axis to a Novel Acute Stress Following Chronic Stress Exposure Modulates Histone Acetylation and the ERK/MAPK Pathway in the Dentate Gyrus of Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2942-2952 ◽  
Author(s):  
Chantelle L. Ferland ◽  
Erin P. Harris ◽  
Mai Lam ◽  
Laura A. Schrader
Keyword(s):  
Dentate Gyrus ◽  
Histone Acetylation ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Male Rats ◽  
Stress Exposure ◽  
Erk Activation ◽  
Acute And Chronic Stress ◽  
Acute Stressor

Evidence suggests that when presented with novel acute stress, animals previously exposed to chronic homotypic or heterotypic stressors exhibit normal or enhanced hypothalamic-pituitary-adrenal (HPA) response compared with animals exposed solely to that acute stressor. The molecular mechanisms involved in this effect remain unknown. The extracellular signal-regulated kinase (ERK) is one of the key pathways regulated in the hippocampus in both acute and chronic stress. The aim of this study was to examine the interaction of prior chronic stress, using the chronic variable stress model (CVS), with exposure to a novel acute stressor (2,5-dihydro-2,4,5-trimethyl thiazoline; TMT) on ERK activation, expression of the downstream protein BCL-2, and the glucocorticoid receptor co-chaperone BAG-1 in control and chronically stressed male rats. TMT exposure after chronic stress resulted in a significant interaction of chronic and acute stress in all 3 hippocampus subregions on ERK activation and BCL-2 expression. Significantly, acute stress increased ERK activation, BCL-2 and BAG-1 protein expression in the dentate gyrus (DG) of CVS-treated rats compared with control, CVS-treated alone, and TMT-only animals. Furthermore, CVS significantly increased ERK activation in medial prefrontal cortex, but acute stress had no significant effect. Inhibition of corticosterone synthesis with metyrapone had no significant effect on ERK activation in the hippocampus; therefore, glucocorticoids alone do not mediate the molecular effects. Finally, because post-translational modifications of histones are believed to play an important role in the stress response, we examined changes in histone acetylation. We found that, in general, chronic stress decreased K12H4 acetylation, whereas acute stress increased acetylation. These results indicate a molecular mechanism by which chronic stress-induced HPA axis plasticity can lead to neurochemical alterations in the hippocampus that influence reactivity to subsequent stress exposure. This may represent an important site of dysfunction that contributes to stress-induced pathology such as depression, anxiety disorders, and posttraumatic stress disorder.

Effects of Castration on Androstenedione, Testosterone and Dihydrotestosterone Plasma Levels in Adult Male Rats

1986 ◽  
Vol 23 (2) ◽  
pp. 122-127 ◽  
Author(s):  
S. Andò ◽  
C. Giacchetto ◽  
M. Canonaco ◽  
S. Aquila ◽  
A. Valenti ◽  
...  
Keyword(s):  
Adult Male ◽  
Plasma Levels ◽  
Male Rats

Prenatal exposure to dexamethasone alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity in adult male rats

2006 ◽  
Vol 290 (5) ◽  
pp. R1366-R1373 ◽  
Author(s):  
Jennifer A. Shoener ◽  
Romana Baig ◽  
Kathleen C. Page
Keyword(s):  
Hpa Axis ◽  
Adult Male ◽  
Restraint Stress ◽  
Exposed Group ◽  
Late Gestation ◽  
Male Rats ◽  
Mrna Levels ◽  
Hypothalamic Pituitary Adrenal ◽  
Hpa Axis Activity ◽  
Circulating Levels

Glucocorticoids are essential for normal hypothalamic-pituitary-adrenal (HPA) axis activity; however, recent studies warn that exposure to excess endogenous or synthetic glucocorticoid during a specific period of prenatal development adversely affects HPA axis stability. We administered dexamethasone (DEX) to pregnant rats during the last week of gestation and investigated subsequent HPA axis regulation in adult male offspring in unrestrained and restraint-stressed conditions. With the use of real-time PCR and RIA, we examined the expression of regulatory genes in the hippocampus, hypothalamus, and pituitary, including corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), glucocorticoid receptors (GR), mineralcorticoid receptors (MR), and 11-β-hydroxysteroid dehydrogenase-1 (11β-HSD-1), as well as the main HPA axis hormones, adrenal corticotropic hormone (ACTH) and corticosterone (CORT). Our results demonstrate that the DEX-exposed group exhibited an overall change in the pattern of gene expression and hormone levels in the unrestrained animals. These changes included an upregulation of CRH in the hypothalamus, a downregulation of MR with a concomitant upregulation of 11β-HSD-1 in the hippocampus, and an increase in circulating levels of both ACTH and CORT relative to unrestrained control animals. Interestingly, both DEX-exposed and control rats exhibited an increase in pituitary GR mRNA levels following a 1-h recovery from restraint stress; however, the increased expression in DEX-exposed rats was significantly less and was associated with a slower return to baseline CORT compared with controls. In addition, circulating levels of ACTH and CORT as well as hypothalamic CRH and hippocampal 11β-HSD-1 expression levels were significantly higher in the DEX-exposed group compared with controls following restraint stress. Taken together, these data demonstrate that late-gestation DEX exposure in rats is associated with persistent changes in both the modulation of HPA axis activity and the HPA axis-mediated response to stress.

Physiological Changes in Androgen Plasma Levels with Elapsing of Time from Castration in Adult Male Rats

1988 ◽  
Vol 20 (02) ◽  
pp. 96-99 ◽  
Author(s):  
S. Ando ◽  
S. Aquila ◽  
E. Beraldi ◽  
M. Canonaco ◽  
M. Panno ◽  
...  
Keyword(s):  
Adult Male ◽  
Plasma Levels ◽  
Male Rats ◽  
Physiological Changes

scholarly journals Voluntary wheel running initially increases adrenal sensitivity to adrenocorticotrophic hormone, which is attenuated with long-term training

2009 ◽  
Vol 106 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Jonathan E. Campbell ◽  
Nasimeh Rakhshani ◽  
Sergiu Fediuc ◽  
Silvio Bruni ◽  
Michael C. Riddell
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Acute Stress ◽  
Wheel Running ◽  
Male Rats ◽  
Voluntary Wheel Running ◽  
Acute Stress Response ◽  
Voluntary Wheel

Although exercise is a common and potent activator of the hypothalamic-pituitary adrenal (HPA) axis, the effects of exercise on the acute stress response are not well understood. Here, we investigated the effects of short- (2 wk) and long-term (8 wk) voluntary wheel running on adrenal sensitivity to ACTH stimulation and the acute stress response to restraint in male rats. Diurnal glucocorticoid patterns were measured on days 7 (all groups) and 35 (8-wk groups). Rats were subjected to 20 min of restraint stress on either week 1 or on week 7 of treatment to assess HPA activation. One week later, exogenous ACTH (75 ng/kg) was administered to assess adrenal sensitivity to ACTH. Following this, adrenals were collected and analyzed for key proteins involved in corticosterone (CORT) synthesis. By the end of week 1, exercising (E) animals had twofold higher peak diurnal CORT levels compared with sedentary (S) animals ( P < 0.01). CORT values were not different between groups at week 8. In response to restraint stress at week 2, CORT values in E were approximately threefold greater than in S ( P < 0.05). No difference was found between E and S rats in the response to, or recovery from, restraint at week 8. During the ACTH challenge at week 2, E demonstrated a ∼2.5-fold increase in adrenal sensitivity compared with S, while no difference was found between E and S at week 8. The expression of steroidogenic acute regulatory protein was found to be ∼50% higher in the adrenals in E compared with S at week 2 ( P < 0.05), but no difference existed between groups at week 8. These results show that volitional wheel running initially causes hyperactivation of the HPA axis, due to enhanced adrenal sensitivity to ACTH, but that these alterations in HPA activity are completely restored by 8 wk of training.

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