scholarly journals Effect of Animal Facility Construction on Basal Hypothalamic-Pituitary-Adrenal and Renin-Aldosterone Activity in the Rat

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1218-1221 ◽  
Author(s):  
Hershel Raff ◽  
Eric D. Bruder ◽  
William E. Cullinan ◽  
Dana R. Ziegler ◽  
Eric P. Cohen
Keyword(s):  
Body Weight ◽  
Stress Hormones ◽  
Construction Project ◽  
Laboratory Animals ◽  
Long Term Effects ◽  
Hypothalamic Pituitary Adrenal ◽  
Facility Construction ◽  
Pituitary Adrenal Axis ◽  
Intense Vibration

Abstract Although loud noise and intense vibration are known to alter the behavior and phenotype of laboratory animals, little is known about the effects of nearby construction. We studied the effect of a nearby construction project on the classic stress hormones ACTH, corticosterone, renin, and aldosterone in rats residing in a barrier animal facility before, for the first 3 months of a construction project, and at 1 month after all construction was completed. During some of the construction, noise and vibrations were not obvious to investigators inside the animal rooms. Body weight matched for age was not altered by nearby construction. During nearby construction, plasma ACTH, corticosterone, and aldosterone were approximately doubled compared with those of pre- and postconstruction levels. Expression of CRH mRNA in the paraventricular nucleus of the hypothalamus, CRH receptor and POMC mRNA in the anterior pituitary, and most mRNAs for steroidogenic genes in the adrenal gland were not significantly changed during construction. We conclude that nearby construction can cause a stress response without long-term effects on hypothalamic-pituitary-adrenal axis gene expression and body weight.

scholarly journals Postnatal Stress in Birds: A Novel Model of Glucocorticoid Programming of the Hypothalamic-Pituitary-Adrenal Axis

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1931-1934 ◽  
Author(s):  
Karen A. Spencer ◽  
Neil P. Evans ◽  
Patricia Monaghan
Keyword(s):  
Stress Response ◽  
Physiological Response ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Long Term Effects ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Postnatal Stress ◽  
Novel Model ◽  
Pituitary Adrenal Axis

There is growing international interest in how environmental conditions experienced during development can shape adult phenotypes and the extent to which such induced changes are adaptive. One physiological system that links an individual to changes in environmental circumstances during development is the hypothalamic-pituitary-adrenal axis. Mammalian studies have linked early postnatal stress to later changes in the hypothalamic-pituitary-adrenal axis; however, the physiological link [lactational corticosterone (CORT) transfer] between mother and offspring during postnatal development constrains the ability to determine the direct effects of such stressors on subsequent physiology and behavior. Here we present a novel model using an avian species, the zebra finch (Taeniopygia guttata), in which maternal hormonal transfer during postnatal development is likely to be absent. Postnatal exposure of chicks to the stress hormone CORT was manipulated for a 16-d period up until nutritional independence (28 d), and the long-term effects on the physiological response to stress determined. CORT doses were scaled to mimic the physiological response of juvenile birds to a capture-handling-restraint protocol. CORT-fed birds showed exaggerated and prolonged responses to acute stress at 60 d of age. Our results clearly demonstrate that postnatal stress has significant long-term effects on the physiological stress response in birds and provides a potential mechanism underlying long-term behavioural responses to developmental conditions. This study represents the first direct evidence for postnatal glucocorticoid programming of the stress response using this novel model for postnatal stress. This model therefore provides an important tool with which to investigate the role of glucocorticoids in shaping adult phenotypes.

scholarly journals Exposure to Δ9-tetrahydrocannabinol during rat pregnancy leads to impaired cardiac dysfunction in postnatal life

2021 ◽  
Author(s):  
Kendrick Lee ◽  
Steven R. Laviolette ◽  
Daniel B. Hardy
Keyword(s):  
Body Weight ◽  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Cardiac Remodelling ◽  
Long Term Effects ◽  
Catch Up ◽  
First Time ◽  
Impaired Cardiac Function ◽  
In Pregnancy

Abstract Background Cannabis use in pregnancy leads to fetal growth restriction (FGR), but the long-term effects on cardiac function in the offspring are unknown, despite the fact that fetal growth deficits are associated with an increased risk of developing postnatal cardiovascular disease. We hypothesize that maternal exposure to Δ9-tetrahydrocannabinol (Δ9-THC) during pregnancy will impair fetal development, leading to cardiac dysfunction in the offspring. Methods Pregnant Wistar rats were randomly selected and administered 3 mg/kg of Δ9-THC or saline as a vehicle daily via intraperitoneal injection from gestational days 6 to 22, followed by echocardiogram analysis of cardiac function on offspring at postnatal days 1 and 21. Heart tissue was harvested from the offspring at 3 weeks for molecular analysis of cardiac remodelling. Results Exposure to Δ9-THC during pregnancy led to FGR with a significant decrease in heart-to-body weight ratios at birth. By 3 weeks, pups exhibited catch-up growth associated with significantly greater left ventricle anterior wall thickness with a decrease in cardiac output. Moreover, these Δ9-THC-exposed offsprings exhibited increased expression of collagen I and III, decreased matrix metallopeptidase-2 expression, and increased inactivation of glycogen synthase kinase-3β, all associated with cardiac remodelling. Conclusions Collectively, these data suggest that Δ9-THC-exposed FGR offspring undergo postnatal catch-up growth concomitant with cardiac remodelling and impaired cardiac function early in life. Impact To date, the long-term effects of perinatal Δ9-THC (the main psychoactive component) exposure on the cardiac function in the offspring remain unknown. We demonstrated, for the first time, that exposure to Δ9-THC alone during rat pregnancy results in significantly smaller hearts relative to body weight. These Δ9-THC-exposed offsprings exhibited postnatal catch-up growth concomitant with cardiac remodelling and impaired cardiac function. Given the increased popularity of cannabis use in pregnancy along with rising Δ9-THC concentrations, this study, for the first time, identifies the risk of perinatal Δ9-THC exposure on early postnatal cardiovascular health.

Suppression of pituitary-testis function in rats treated neonatally with a gonadotrophin-releasing hormone agonist and antagonist: acute and long-term effects

1989 ◽  
Vol 123 (1) ◽  
pp. 83-91 ◽  
Author(s):  
K.-L. Kolho ◽  
I. Huhtaniemi
Keyword(s):  
Body Weight ◽  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Long Term Effects ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Accessory Sex Organs ◽  
Gonadotrophin Releasing Hormone

ABSTRACT The acute and long-term effects of pituitary-testis suppression with a gonadotrophin-releasing hormone (GnRH) agonist, d-Ser(But)6des-Gly10-GnRH N-ethylamide (buserelin; 0·02, 0·1, 1·0 or 10 mg/kg body weight per day s.c.) or antagonist, N-Ac-d-Nal(2)1,d-p-Cl-Phe2,d-Trp3,d-hArg(Et2)6,d-Ala10-GnRH (RS 68439; 2 mg/kg body weight per day s.c.) were studied in male rats treated on days 1–15 of life. The animals were killed on day 16 (acute effects) or as adults (130–160 days; long-term effects). Acutely, the lowest dose of the agonist decreased pituitary FSH content and testicular LH receptors, but with increasing doses pituitary and serum LH concentrations, intratesticular testosterone content and weights of testes were also suppressed (P< 0·05–0·01). No decrease was found in serum FSH or in weights of accessory sex organs even with the highest dose of the agonist, the latter finding indicating continuing secretion of androgens. The GnRH antagonist treatment suppressed pituitary LH and FSH contents and serum LH (P< 0·05–0·01) but, as with the agonist, serum FSH remained unaltered. Testicular testosterone and testis weights were decreased (P <0·01) but testicular LH receptors remained unchanged. Moreover, the seminal vesicle and ventral prostate weights were reduced, in contrast to the effects of the agonists. Pituitary LH and FSH contents had recovered in all adult rats treated neonatally with agonist and there was no effect on serum LH and testosterone concentrations or on fertility. In contrast, in adult rats treated neonatally with antagonist, weights of testis and accessory sex organs remained decreased (P <0·01–0·05) but hormone secretion from the pituitary and testis had returned to normal except that serum FSH was increased by 80% (P <0·01). Interestingly, 90% of the antagonist-treated animals were infertile. It is concluded that treatment with a GnRH agonist during the neonatal period does not have a chronic effect on pituitary-gonadal function. In contrast, GnRH antagonist treatment neonatally permanently inhibits the development of the testis and accessory sex organs and results in infertility. Interestingly, despite the decline of pituitary FSH neonatally, neither of the GnRH analogues was able to suppress serum FSH values and this differs from the concomitant changes in LH and from the effects of similar treatments in adult rats. Journal of Endocrinology (1989) 123, 83–91

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