scholarly journals Postnatal Aromatase Blockade Increases c-fos mRNA Responses to Acute Restraint Stress in Adult Male Rats

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1603-1608 ◽  
Author(s):  
Brenda Bingham ◽  
Nancy X. R. Wang ◽  
Leyla Innala ◽  
Victor Viau
Keyword(s):  
Adult Male ◽  
Restraint Stress ◽  
Neonatal Period ◽  
Male Rats ◽  
Neural Pathways ◽  
Somatosensory Processing ◽  
Estrogen Exposure ◽  
Old Adult ◽  
Neuroendocrine Responses ◽  
Fos Expression

Recent evidence suggests that the aromatization of testosterone to estrogen is important for the organizing effects of neonatal testosterone on neuroendocrine responses to acute challenges. However, the extent to which neonatal inhibition of aromatase alters the stress-induced activation of neural pathways has not been examined. Here we assessed central patterns of c-fos mRNA induced by 30 min of restraint in 65-d-old adult male rats that were implanted with sc capsules of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD), introduced within 12 h of birth and removed on d 21 of weaning. Neonatal ATD decreased the expression of arginine vasopressin within extrahypothalamic regions in adults, confirming reduced estrogen exposure during development. As adults, ATD-treated animals showed higher corticosterone responses at 30 min of restraint exposure compared with control animals as well as higher c-fos expression levels in the paraventricular nucleus of the hypothalamus. ATD treatment also increased stress-induced c-fos within several limbic regions of the forebrain, in addition to areas involved in somatosensory processing. Based on these results, we propose that the conversion of testosterone to estrogen during the neonatal period exerts marked, system-wide effects to organize adult neuroendocrine responses to homeostatic threat.

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.

Prenatal immobilization stress and postnatal maternal separation cause differential neuroendocrine responses to fasting stress in adult male rats

2019 ◽  
Vol 62 (6) ◽  
pp. 737-748 ◽  
Author(s):  
Angélica Roque ◽  
Roberto Ruiz‐González ◽  
Edel Pineda-López ◽  
Luz Torner ◽  
Naima Lajud
Keyword(s):  
Adult Male ◽  
Maternal Separation ◽  
Immobilization Stress ◽  
Male Rats ◽  
Neuroendocrine Responses

The AT-1 Angiotensin Receptor is Involved in the Autonomic and Neuroendocrine Responses to Acute Restraint Stress in Male Rats

2021 ◽  
Author(s):  
Taíz F. S. Brasil ◽  
Ivaldo J. A. Belém-Filho ◽  
Eduardo A. T. Fortaleza ◽  
José Antunes-Rodrigues ◽  
Fernando M. A. Corrêa
Keyword(s):  
Restraint Stress ◽  
Male Rats ◽  
Angiotensin Receptor ◽  
Acute Restraint Stress ◽  
Neuroendocrine Responses

scholarly journals Olfactory Discrimination in Adult Male Rats Undernourished during the Pre- and Neonatal Period

2012 ◽  
Vol 02 (03) ◽  
pp. 283-290 ◽  
Author(s):  
Mitzi G. Carreon ◽  
Carmen Torrero ◽  
Mirelta Regalado ◽  
Lorena Rubio ◽  
Manuel Salas
Keyword(s):  
Adult Male ◽  
Neonatal Period ◽  
Olfactory Discrimination ◽  
Male Rats

scholarly journals Chronic Restraint Stress Inhibits the Response to a Second Hit in Adult Male Rats: A Role for BDNF Signaling

2020 ◽  
Vol 21 (17) ◽  
pp. 6261 ◽  
Author(s):  
Paola Brivio ◽  
Giulia Sbrini ◽  
Giulia Corsini ◽  
Maria Serena Paladini ◽  
Giorgio Racagni ◽  
...  
Keyword(s):  
Adult Male ◽  
Restraint Stress ◽  
Stressful Events ◽  
Male Rats ◽  
Chronic Restraint Stress ◽  
Sprague Dawley ◽  
Second Hit ◽  
Bdnf Signaling ◽  
Intracellular Cascades ◽  
Challenging Situation

Depression is a recurrent disorder, with about 50% of patients experiencing relapse. Exposure to stressful events may have an adverse impact on the long-term course of the disorder and may alter the response to a subsequent stressor. Indeed, not all the systems impaired by stress may normalize during symptoms remission, facilitating the relapse to the pathology. Hence, we investigated the long-lasting effects of chronic restraint stress (CRS) and its influence on the modifications induced by the exposure to a second hit on brain-derived neurotrophic factor (BDNF) signaling in the prefrontal cortex (PFC). We exposed adult male Sprague Dawley rats to 4 weeks of CRS, we left them undisturbed for the subsequent 3 weeks, and then we exposed animals to one hour of acute restraint stress (ARS). We found that CRS influenced the release of corticosterone induced by ARS and inhibited the ability of ARS to activate mature BDNF, its receptor Tropomyosin receptor kinase B (TRKB), and their associated intracellular cascades: the TRKB-PI3K-AKT), the MEK-MAPK/ERK, and the Phospholipase C γ (PLCγ) pathways, positively modulated by ARS in non-stressed animals. These results suggest that CRS induces protracted and detrimental consequences that interfere with the ability of PFC to cope with a challenging situation.

Cold exposure attenuates effects of secretagogues on serum prolactin and growth hormone levels in male rats

1995 ◽  
Vol 268 (4) ◽  
pp. E758-E765
Author(s):  
P. Rauhala ◽  
J. J. Idanpaan-Heikkila ◽  
A. Lang ◽  
R. K. Tuominen ◽  
P. T. Mannisto
Keyword(s):  
Growth Hormone ◽  
Cold Exposure ◽  
Restraint Stress ◽  
Prolactin Secretion ◽  
Kappa Opioid Receptor ◽  
Male Rats ◽  
Serum Prolactin ◽  
Dopamine Antagonist ◽  
Neural Pathways ◽  
Gh Secretion

The stimulatory effect of morphine, dexmedetomidine (an alpha 2-adrenoceptor agonist), 1-(3-chlorophenyl)-piperazine (m-CPP, a 5-HT1B agonist), U-50488H (a kappa-opioid receptor agonist), pimozide (a dopamine antagonist), and restraint stress on prolactin and growth hormone (GH) secretion was compared during cold exposure (4 degrees C) and under basal conditions (30 degrees C) in male rats. Rectal temperature was also measured. The stimulatory effect of morphine, dexmedetomidine, m-CPP, and partially U-50488H on prolactin secretion was attenuated in rats kept at 4 degrees C. Cold exposure did not abolish prolactin release induced by pimozide and restraint stress. Cold exposure also antagonized the effect of morphine and dexmedetomidine on GH secretion. The stimulatory effect of morphine on prolactin and GH secretion was restored in the warm environment despite the sustained hypothermia. Cold exposure blocked the stimulatory effect of morphine on prolactin secretion in rats that were tolerant to the hypothermic effect of morphine. Thus hypothermia caused by morphine, dexmedetomidine, and m-CPP during cold exposure is not the sole factor in the antagonistic effect of cold. We suggest that cold exposure releases some compound(s) modulating hypothalamic neural pathways.

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