Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats

2013 ◽  
Vol 219 (2) ◽  
pp. 89-100 ◽  
Author(s):  
Anna Fodor ◽  
Ottó Pintér ◽  
Ágnes Domokos ◽  
Kristina Langnaese ◽  
István Barna ◽  
...  
Keyword(s):  
Stress State ◽  
Adrenal Gland ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Mrna Levels ◽  
Brattleboro Rats ◽  
Physiological Changes ◽  
Pregnancy And Lactation

Adaptation to stress is a basic phenomenon in mammalian life that is mandatorily associated with the activity of the hypothalamic–pituitary–adrenal (HPA) axis. An increased resting activity of the HPA axis can be measured during pregnancy and lactation, suggesting that these reproductive states lead to chronic load in females. In this study, we examined the consequences of the congenital lack of vasopressin on the activity of the HPA axis during lactation using vasopressin-deficient Brattleboro rats. Virgin and lactating, homozygous vasopressin-deficient rats were compared with control, heterozygous rats. In control dams compared with virgins, physiological changes similar to those observed in a chronic stress state (thymus involution, adrenal gland hyperplasia, elevation of proopiomelanocortin mRNA levels in the adenohypophysis, and resting plasma corticosterone levels) were observed. In vasopressin-deficient dams, adrenal gland hyperplasia and resting corticosterone level elevations were not observed. Corticotropin-releasing hormone (Crh) mRNA levels in the hypothalamic paraventricular nucleus were elevated in only the control dams, while oxytocin (OT) mRNA levels were higher in vasopressin-deficient virgins and lactation induced a further increase in both the genotypes. Suckling-induced ACTH and corticosterone level elevations were blunted in vasopressin-deficient dams. Anaphylactoid reaction (i.v. egg white) and insulin-induced hypoglycemia stimulated the HPA axis, which were blunted in lactating rats compared with the virgins and in vasopressin-deficient rats compared with the controls without interaction of the two factors. Vasopressin seems to contribute to the physiological changes observed during lactation mimicking a chronic stress state, but its role in acute HPA axis regulation during lactation seems to be similar to that observed in virgins. If vasopressin is congenitally absent, OT, but not the CRH, compensates for the missing vasopressin; however, the functional restitution remains incomplete.

Maternal high fat diet during critical windows of development alters adrenal cortical and medullary enzyme expression in adult male rat offspring

2010 ◽  
Vol 1 (4) ◽  
pp. 245-254 ◽  
Author(s):  
K. L. Connor ◽  
M. H. Vickers ◽  
C. Cupido ◽  
E. Sirimanne ◽  
D. M. Sloboda
Keyword(s):  
Leptin Receptor ◽  
Maternal Nutrition ◽  
Inhibitory Effect ◽  
Plasma Corticosterone ◽  
Male Rat ◽  
Chow Diet ◽  
Mrna Levels ◽  
High Fat ◽  
Adrenal Steroidogenesis ◽  
Pregnancy And Lactation

We previously reported that a maternal high fat (HF) diet resulted in adult offspring with increased adiposity and hyperleptinemia. As leptin has an inhibitory effect on adrenal steroidogenesis and a stimulatory effect on epinephrine synthesis, we hypothesized that key adrenal steroidogenic and catecholaminergic enzymes would be altered in these offspring. Wistar rats were randomized into three groups at weaning: (1) control dams fed a standard control chow diet from weaning and throughout pregnancy and lactation (CON), (2) dams fed a HF diet from weaning and throughout pregnancy and lactation (MHF) and (3) dams fed standard control chow diet throughout life until conception, then fed a HF diet in pregnancy and lactation (PLHF). Dams were mated at day 100 (P100). After birth at P22 (weaning), male offspring were fed a standard control chow (con) or high fat (hf) diet. At P160, plasma samples and adrenal tissues were collected. Postweaning hf diet significantly elevated plasma corticosterone concentrations in PLHF-hf offspring compared to PLHF-con. MHF nutrition increased adrenal adrenocorticotrophic hormone receptor (ACTH-R) mRNA levels compared to CON-con. 3β-hydroxysteroid dehydrogenase (3βHSD) mRNA levels were decreased in MHF compared to PLHF offspring. Phenylethanolamine N-methyltransferase (PNMT) mRNA levels were increased in MHF-hf offspring compared to MHF-con. Plasma homocysteine (HCY) concentrations were significantly elevated in CON-hf and MHF-hf offspring compared to chow-fed offspring, associated with elevated intakes of methionine and reduced intakes of pyridoxine. Immunoreactive leptin receptor (ObRb) and PNMT were colocalized in medullary chromaffin cells. This study suggests that a postweaning HF diet in offspring induced changes in adrenal gene expression levels that are dependent upon the level of maternal nutrition.

Carbaryl-induced elevation of corticosterone level and cholinergic mechanism

1983 ◽  
Vol 3 (10) ◽  
pp. 973-977 ◽  
Author(s):  
S. K. Ray ◽  
M. K. Poddar
Keyword(s):  
Single Dose ◽  
Adrenal Gland ◽  
Rat Brain ◽  
Corticosterone Level ◽  
Acetylcholinesterase Activity ◽  
Plasma Corticosterone ◽  
Significant Rise ◽  
Atropine Sulphate ◽  
Transaminase Activity ◽  
Cholinergic Mechanism

Administration of a single dose (200 mg/kg, p.o.) of carbaryl to rats produced a significant rise in adrenal and plasma corticosterone levels and an increase of tyrosine α-ketoglutarate transaminase activity in the liver cytosot. Synaptosomal acetylcholinesterase activity of the hypothalamic and the striatal regions of rat brain was decreased by carbaryl treatment under similar conditions. Pretreatment (0.5 h) with atropine sulphate (10 mg/kg, i.p.) failed to counteract the carbaryl-induced elevation of adrenal and plasma corticosterone levels and hence the liver tyrosine α-ketoglutarate transaminase activity. Present results suggest that the carbaryl-induced rise in the corticosterone level in the adrenal gland and plasma is not due to a cholinergic mechanism.

scholarly journals Inflammatory Pain and Corticosterone Response in Infant Rats: Effect of 5-HT1A Agonist Buspirone Prior to Gestational Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Inflammatory Pain ◽  
Formalin Test ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Corticosterone Level ◽  
Infant Rats ◽  
Corticosterone Response ◽  
Gestational Stress

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.

scholarly journals Differential Adaptive Responses to Chronic Stress of Maternally Stressed Male Mice Offspring

Endocrinology ◽  
2005 ◽  
Vol 146 (7) ◽  
pp. 3202-3210 ◽  
Author(s):  
Sooyoung Chung ◽  
Gi Hoon Son ◽  
Sung Ho Park ◽  
Eonyoung Park ◽  
Kun Ho Lee ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Feedback Inhibition ◽  
Corticosterone Level ◽  
Dependent Manner ◽  
Male Mice ◽  
Adaptive Responses ◽  
Repeated Restraint Stress ◽  
Postnatal Stress

Abstract It is well established that stress in early life can alter the activity of the hypothalamus-pituitary-adrenal (HPA) axis, but most studies to date have focused on HPA reactivity in response to a single acute stress. The present study addressed whether stress in pregnant mice could influence the adaptive responses of their offspring to chronic stress. Male offspring were exclusively used in this study. Elevated plus maze tests revealed that 14 d of repeated restraint stress (6 h per day; from postnatal d 50–63) significantly increased anxiety-like behavior in maternally stressed mice. NBI 27914, a CRH receptor antagonist, completely eliminated anxiety-related behaviors in a dose-dependent manner, indicating an involvement of a hyperactive CRH system. In accordance with increased anxiety, CRH contents in the hypothalamus and amygdala were significantly higher in these mice. Despite an increased basal activity of the CRH-ACTH system, the combination of chronic prenatal and postnatal stress resulted in a significant reduction of basal plasma corticosterone level, presumably because of a defect in adrenal function. Along with alterations in hypothalamic and hippocampal corticosteroid receptors, it was also demonstrated that a dysfunction in negative feedback inhibition of the HPA axis could be deteriorated by chronic stress in maternally stressed male mice. Taken together, these results indicate that exposure to maternal stress in the womb can affect an animal’s coping capacity to chronic postnatal stress.

Neonatal monosodium glutamate treatment alters both the activity and the sensitivity of the rat hypothalamo-pituitary-adrenocortical axis

1994 ◽  
Vol 141 (3) ◽  
pp. 497-503 ◽  
Author(s):  
P J Larsen ◽  
J D Mikkelsen ◽  
D Jessop ◽  
S L Lightman ◽  
H S Chowdrey
Keyword(s):  
Hpa Axis ◽  
Restraint Stress ◽  
Acute Stress ◽  
Monosodium Glutamate ◽  
Plasma Corticosterone ◽  
Mrna Levels ◽  
Plasma Acth ◽  
Corticotrophin Releasing Factor ◽  
Acute And Chronic Stress ◽  
Corticosterone Response

Abstract We have investigated the effects of monosodium glutamate (MSG) lesioning of the arcuate nucleus on both central and peripheral components of the hypothalamo-pituitary-adrenocortical (HPA) axis under basal conditions and under acute and chronic stress. Plasma ACTH levels were lower in MSG-lesioned rats (27 ± 7 pg/ml) compared with controls (71 ± 18 pg/ml) while corticosterone levels were elevated (523 ± 84 ng/ml compared with 176 ± 34 ng/ml). Quantititative in situ hybridization histochemistry revealed that corticotrophin-releasing factor mRNA levels in the medial parvocellular part of the hypothalamic paraventricular nucleus were significantly lower in MSG-treated rats. MSG lesioning resulted in an enhanced response of corticosterone to restraint stress (1309 ± 92 ng/ml compared with 628 ± 125 ng/ml in sham-lesioned animals), while ACTH responses to restraint stress in MSG-lesioned and sham-MSG groups were not significantly different (160 ± 24 pg/ml and 167 ± 24 pg/ml respectively). These data suggest that MSG-lesioned rats have an increased adrenocortical sensitivity. In rats subjected to the chronic osmotic stimulus of drinking 2% saline for 12 days, plasma ACTH levels were significantly reduced (15 ± 5 pg/ml) and the ACTH and corticosterone responses to restraint stress were eliminated. ACTH levels were also reduced in MSG-treated animals given 2% saline and the ACTH response to acute stress remained absent in these animals. However, a robust corticosterone response to restraint stress was observed in saline-treated MSG-lesioned rats. These data demonstrate that MSG lesioning results in elevated basal and stress-induced plasma corticosterone, and restores the adrenocortical response to stress which is absent in chronically osmotically stimulated rats. The evidence is consistent with the suggestion that MSG lesions a pathway involved in tonic inhibition of the HPA axis. In addition, the adrenocortical sensitivity to ACTH and other secretagogues may be increased in MSG-treated animals. Journal of Endocrinology (1994) 141, 497–503

scholarly journals Electro-Acupuncture Attenuates Chronic Stress Responses via Up-Regulated Central NPY and GABAA Receptors in Rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Yu Yang ◽  
Haijie Yu ◽  
Reji Babygirija ◽  
Bei Shi ◽  
Weinan Sun ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Mrna Expression ◽  
Motor Function ◽  
Hpa Axis ◽  
Stress Responses ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Gamma Aminobutyric Acid ◽  
Motor Functions ◽  
Gastric Motor Function

Stress can increase the release of corticotropin-releasing factor (CRF) in the hypothalamus, resulting in attenuation of gastric motor functions. In contrast, central neuropeptide Y (NPY) can reduce the biological actions of CRF, and in turn weaken stress responses. Although electroacupuncture (EA) at stomach 36 (ST-36) has been shown to have anti-stress effects, its mechanism has not yet been investigated. The effect of EA at ST-36 on the hypothalamus-pituitary-adrenal (HPA) axis and gastrointestinal motility in chronic complicated stress (CCS) conditions have not been studied and the inhibitory mechanism of NPY on CRF through the gamma-aminobutyric acid (GABA)A receptor need to be further investigated. A CCS rat model was set up, EA at ST-36 was applied to the bilateral hind limbs every day prior to the stress loading. Further, a GABAA receptor antagonist was intracerebroventricularly (ICV) injected daily. Central CRF and NPY expression levels were studied, serum corticosterone and NPY concentrations were analyzed, and gastric motor functions were assessed. CCS rats showed significantly elevated CRF expression and corticosterone levels, which resulted in inhibited gastric motor functions. EA at ST-36 significantly increased central NPY mRNA expression and reduced central CRF mRNA expression as well as the plasma corticosterone level, helping to restore gastric motor function. However, ICV administration of the GABAA receptor antagonist significantly abolished these effects. EA at ST-36 upregulates the hypothalamic NPY system. NPY may, through the GABAA receptor, significantly antagonize the overexpressed central CRF and attenuate the HPA axis activities in CCS conditions, exerting influences and helping to restore gastric motor function.

scholarly journals Secretagogin Mediates the Regulatory Effect of Electroacupuncture on Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Surgical Trauma

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Mizhen Zhang ◽  
Jingxian Sun ◽  
Yu Wang ◽  
Zhanzhuang Tian
Keyword(s):  
Hpa Axis ◽  
Plasma Corticosterone ◽  
Control Group ◽  
Surgical Trauma ◽  
Mrna Levels ◽  
Hypothalamic Pituitary Adrenal ◽  
Protein Levels ◽  
Polymerase Chain ◽  
Hepatectomy Group

Electroacupuncture (EA) improves hypothalamic-pituitary-adrenal (HPA) axis disorder by reducing corticotropin-releasing hormone (CRH) synthesis and release in the paraventricular nucleus (PVN). However, the potential mechanism underlying CRH regulation remains unclear. Secretagogin (SCGN) is closely related to stress and is involved in regulating the release of CRH. We hypothesized that SCGN in the PVN might trigger the HPA system and be involved in EA-mediated modulation of HPA dysfunction caused by surgical trauma. Serum CRH and adrenocorticotropic hormone (ACTH) and plasma corticosterone (CORT) levels at 6 h and 24 h after hepatectomy were determined by radioimmunoassay. CRH and SCGN protein levels in the PVN were detected by western blot and immunofluorescence, and CRH and SCGN mRNA levels in the PVN were determined by means of real-time polymerase chain reaction (RT-PCR) and in situ hybridization (ISH). Our studies showed that serum CRH, ACTH, and CORT levels and PVN CRH expression were significantly increased at 6 h and 24 h after hepatectomy in the hepatectomy group compared with the control group, and those in the EA+hepatectomy group were decreased compared with those in the hepatectomy group. The protein and mRNA levels of SCGN in the PVN were also increased after hepatectomy, and their expression in the EA+hepatectomy group was decreased compared with that in the hepatectomy group. When SCGN expression in the PVN was functionally knocked down by a constructed CsCI virus, we found that SCGN knockdown decreased the serum CRH, ACTH, and CORT levels in the SCGN shRNA+hepatectomy group compared with the hepatectomy group, and it also attenuated CRH expression in the PVN. In summary, our findings illustrated that EA normalized HPA axis dysfunction after surgical trauma by decreasing the transcription and synthesis of SCGN.

scholarly journals TheKampoMedicine Yokukansan Decreases MicroRNA-18 Expression and Recovers Glucocorticoid Receptors Protein Expression in the Hypothalamus of Stressed Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Shoko Shimizu ◽  
Takashi Tanaka ◽  
Takashi Takeda ◽  
Masaya Tohyama ◽  
Shingo Miyata
Keyword(s):  
Hpa Axis ◽  
Stress Responses ◽  
Glucocorticoid Receptors ◽  
Psychological Symptoms ◽  
Plasma Corticosterone ◽  
Mrna Levels ◽  
Stress Exposure ◽  
Protein Levels ◽  
Hpa Axis Activity ◽  
The Brain

It is well known that glucocorticoid receptor (GR) signaling regulates the hypothalamic-pituitary-adrenal (HPA) axis, and GR expression level is associated with HPA axis activity. Recent studies revealed that microRNA- (miR-) 18 and/or 124a are candidate negative regulators of GR in the brain. TheKampomedicine Yokukansan (YKS) can affect psychological symptoms such as depression and anxiety that are associated with stress responses. In this study, we evaluated the effect of YKS on miR-18 and 124a and GR levels in mice exposed to stress. We found that YKS pretreatment normalized elevated plasma corticosterone levels in stress-exposed mice. In addition, GR mRNA levels were downregulated in the brain following stress exposure. While miR-124a expression levels were not altered in the hypothalamus of stress-exposed mice, miR-18 levels decreased in the hypothalamus of YKS-pretreated mice after stress exposure. Finally, GR protein levels in the paraventricular nucleus (PVN) of the hypothalamus after stress exposure recovered in YKS-pretreated mice. Collectively, these data suggest that YKS normalizes GR protein levels by regulating miR-18 expression in the hypothalamus, thus normalizing HPA axis activity following stress exposure.

scholarly journals Lateral Hypothalamus Corticotropin Releasing Hormone Receptor-1 Inhibition Modulates Stress- Induced Anxiety Behavior

2021 ◽  
Author(s):  
Masoumeh Eghtesad ◽  
◽  
Mahmoud Elahdadi Salmani ◽  
Taghi Lashkarbolouki ◽  
Iran Goudarzi1 ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Acute Stress ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Area ◽  
Releasing Hormone ◽  
Male Wistar Rats ◽  
Induced Changes ◽  
Crh Receptor Type 1

Stress is a reaction to unwanted events disturbing body homeostasis which influences its pathways and target areas. Stress affects the brain through the lateral hypothalamic area (LHA) orexinergic system that mediates the effect of corticotropin-releasing hormone (CRH) through CRH receptor type 1 (CRHr1). Therefore, this study explores the outcome of stress exposure on anxiety development and the involvement of the LHA through LHA-CRHr1. Male Wistar rats (220-250g) implanted with a cannula in either side of the LHA received acute or chronic stress. Subsequently, exploratory behavior and anxiety was examined using the open field (OF) and elevated plus maze (EPM), respectively. Prior to sacrifice, the cerebrospinal fluid (CSF) and the blood were sampled. Nissl stain was performed on fixed brain tissues. Acute stress resulted in a decrease of exploration in the OF and an increase of anxiety in the EPM. LHA-CRHr1 inhibition reversed the variables to increase the exploration and decrease the anxiety. In contrast, chronic stress did not show any effect on the anxiety-related behaviors. Chronic stress decreased the cell population in the LHA, which was prevented by the CRHr1 inhibition. However, the CRHr1 inhibition was unable to reverse the chronic stress increase of the CSF orexin level. Furthermore, both acute and chronic stresses increased the plasma corticosterone level and only the CRHr1 inhibition impeded the effect. Our results recognize LHA-CRHr1 as a capable candidate modulating acute stress-induced anxiety development and chronic stress-induced changes in the cellular population of the region.

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