Sex-specific effects of prenatal stress on hypothalamic-pituitary-adrenal responses to stress and brain glucocorticoid receptor density in adult rats

McCormick, Cheryl M.; Smythe, James W.; Sharma, Shakti; Meaney, Michael J.

doi:10.1016/0165-3806(94)00153-q

Cited by 436 publications

(273 citation statements)

References 29 publications

Supporting

Mentioning

247

Contrasting

Unclassified

Order By: Relevance

“…Indeed, PS females show a higher ACTH response to acute stress than female controls, while PS males show a faster recovery of stress-induced ACTH increase than control males (McCormick et al, 1995). PS males have even been reported to present reduced corticosteroid receptors density in the cerebral cortex, while female PS rats show an increased density (McCormick et al, 1995). Therefore, the behavioral performances of PS animals, and notably sex-related differences, may markedly depend upon stressful stimuli and emotional state of animals performing the behavioral examination.…”

Section: J Meunier Et Almentioning

confidence: 97%

“…The important sex-related differences observed in the hormonal response to PS may in part be related to the discrepancies observed in memory tests, since most of them, including the water-maze or passive avoidance response, involve stressful stimuli. Indeed, PS females show a higher ACTH response to acute stress than female controls, while PS males show a faster recovery of stress-induced ACTH increase than control males (McCormick et al, 1995). PS males have even been reported to present reduced corticosteroid receptors density in the cerebral cortex, while female PS rats show an increased density (McCormick et al, 1995).…”

Section: J Meunier Et Almentioning

confidence: 99%

See 1 more Smart Citation

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Meunier

Gué

Récasens

et al. 2004

British J Pharmacology

View full text Add to dashboard Cite

1 Stress during pregnancy results in complex neurochemical and behavioral alterations throughout the offspring lifetime. We here examined the impact of prenatal stress (PS) on memory functions in male and female offspring and report the efficacy of a selective sigma 1 (s 1 ) receptor agonist, igmesine, in alleviating the observed deficits. 2 Dams received an unpredictable 90-min duration restraint stress from gestational day E17 to E20. Learning was examined in offspring between day P24 and P36 using spontaneous alternation in the Y-maze, delayed alternation in the T-maze, water-maze learning and passive avoidance. 3 Both male and female PS rats showed impairments of spontaneous and delayed alternation performances. Acquisition of a fixed platform position in the water-maze was unchanged in PS rats, but the probe test revealed a diminution of time spent in the training quadrant. Acquisition of a daily changing platform position demonstrated impaired working memory for male and female PS rats. Finally, passive avoidance deficits were observed. 4 Pretreatment with the selective s 1 agonist igmesine (1-10 mg kg À1 i.p.) reversed the PS-induced learning deficits in offspring rats for each test. The s 1 antagonist BD1063 failed to affect performances alone but blocked the igmesine effect, confirming the involvement of the s 1 receptor. 5 PS thus induces delayed memory deficits, affecting spatial and nonspatial, short-and long-term memories in juvenile male and female offspring rats. Activation of the s 1 neuromodulatory receptor allows a significant recovery of the memory functions in PS rats.

show abstract

Section: J Meunier Et Almentioning

confidence: 97%

Section: J Meunier Et Almentioning

confidence: 99%

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Meunier

Gué

Récasens

et al. 2004

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Specifically, female rats appear to be more responsive to the effects of prenatal exposure to maternal psychosocial stress (e.g., restraint), exhibiting hypocorticism over the diurnal cycle, as well as increased ACTH and cortisol responses to restraint in adulthood (Koehl et al, 1999;McCormick, Smythe, Sharma, & Meaney, 1995). Moreover, data from mouse models suggest that there may be greater transport of corticosterone across the placenta for female versus male fetuses (Montano, Wang, & vom Saal, 1993); however, female guinea pigs exposed prenatally to dexamathasone showed increases in plasma cortisol levels only during the follicular and luteal phases of the cycles, suggesting a potential influence of sex steroids in the increased cortisol responses of females exposed to prenatal stress (Liu, Li, & Matthews, 2001).…”

Section: Discussionmentioning

confidence: 99%

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Ellman

Schetter

Hobel

et al. 2008

Developmental Psychobiology

154

146

View full text Add to dashboard Cite

The purpose of the study was to determine the specific periods during pregnancy in which human fetal exposure to stress hormones affects newborn physical and neuromuscular maturation. Blood was collected from 158 women at 15, 19, 25, and 31 weeks' gestation. Levels of placental corticotropin-releasing hormone (CRH) and maternal cortisol were determined from plasma. Newborns were evaluated with the New Ballard Maturation Score. Results indicated that increases in maternal cortisol at 15, 19, and 25 weeks and increases in placental CRH at 31 weeks were significantly associated with decreases in infant maturation among males (even after controlling for length of gestation). Results also suggested that increases in maternal cortisol at 31 weeks were associated with increases in infant maturation among females, although these results were not significant after controlling for length of gestation. Findings suggest that stress hormones have effects on human fetal neurodevelopment that are independent of birth outcome.

show abstract

“…Women are more likely than men to develop depression following a stressful life event early in life 300 and their HPA axis is more susceptible to PS-induced programming. [301][302][303] Women have a lower mean rate of 5-HT synthesis compared to men, while men and women appear to have similar stores of brain 5-HT. 109 Thus, in times of increased 5-HT utilization, a lower rate of synthesis in women may cause 5-HT levels to decline more in women than in men, possibly increasing vulnerability to depression.…”

Section: Biopsychological Interactionsmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

View full text Add to dashboard Cite

In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

show abstract

Sex-specific effects of prenatal stress on hypothalamic-pituitary-adrenal responses to stress and brain glucocorticoid receptor density in adult rats

Cited by 436 publications

References 29 publications

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Contact Info

Product

Resources

About

Sex-specific effects of prenatal stress on hypothalamic-pituitary-adrenal responses to stress and brain glucocorticoid receptor density in adult rats

Cited by 436 publications

References 29 publications

Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Contact Info

Product

Resources

About

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats