Effects of Prenatal Stress on the Activity of an Enzyme Involved in Neurosteroid Synthesis During the “Critical Period” of Sexual Differentiation of the Brain in Male Rats

Ordyan, N. É.; Pivina, S. G.

doi:10.1007/s11055-005-0148-4

Cited by 17 publications

(23 citation statements)

References 24 publications

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“…This timing coincides with the peak of the neonatal testosterone surge, which is known to have important long-term effects on CNS function and behavior. The increase in neonatal testosterone due to birth hypoxia contrasts with the effects of many other manipulations, including neonatal cooling or anesthesia and maternal exposure to repeated hypoxia, stress, alcohol or toxins during pregnancy, which have been reported to decrease neonatal testosterone [9,10,11,12,13]. Birth hypoxia has been shown to be associated with alterations in levels of a wide variety of circulating hormones [15,16,17,18,19].…”

Section: Discussionmentioning

confidence: 99%

“…The testosterone antibody provided has low cross-reactivity with other androgens (5α-dihydrotestosterone 3.4%; 5α-androstane-3β, 17β-diol 2.2%; 11-oxotestosterone 2.0%; all other androgens <1.0%). Given this low cross-reactivity, data are referred to as plasma testosterone, although plasma samples were not chromatographically separated [11]. All samples were assayed in duplicate, with a lower limit of sensitivity of the assay of 0.08 ng/ml.…”

Section: Methodsmentioning

confidence: 99%

“…This increase in testosterone at a critical period of development has been implicated in the long-term modulation of a number of central nervous system (CNS) functions including play and sexual behavior, dopaminergic neurotransmission and responses to early CNS lesions [3,4,5,6,7,8]. The neonatal testosterone surge is relatively labile in that it has been shown to be altered by environmental manipulations such as cooling or anesthesia in the neonate and maternal exposure to repeated hypoxia, stress, alcohol or toxins during pregnancy [9,10,11,12,13]. In the current study we examined whether neonatal testosterone levels can be influenced by another environmental insult, namely birth hypoxia.…”

Section: Introductionmentioning

confidence: 99%

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Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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Background/Aims: Global birth hypoxia in rats has been shown to produce long-term changes in central nervous system functions, known to be influenced by neonatal testosterone secretion. Birth hypoxia alters levels of several circulating hormones, but it is unknown if it affects neonatal testosterone. Methods: Using a rat model of acute global hypoxia during cesarean section (C-section) birth, this study tested whether birth hypoxia affects neonatal testosterone. We then evaluated whether the observed hypoxia-induced changes in neonatal testosterone may be mediated via N-methyl-D-aspartate (NMDA) receptor activation and/or altered luteinizing hormone (LH), adrenocorticotropic hormone (ACTH) or corticosterone levels. Longer-term effects of birth hypoxia on testosterone-related function were also assessed. Results: Rats born by C-section + 15 min of anoxia had significantly higher plasma testosterone at 2 and 3 h after birth compared to controls born either vaginally or by C-section. Administration of an NMDA receptor antagonist at birth increased neonatal testosterone in both anoxic pups and controls. Pups exposed to birth anoxia under hypothermic conditions also showed increased neonatal testosterone. Circulating LH, follicle-stimulating hormone and corticosterone in neonates, and testosterone at adulthood were unaffected by birth hypoxia. However, plasma ACTH was significantly increased in anoxic neonates at 2 h after birth. Birth condition had no effect on anogenital distance or juvenile play behavior. Conclusion: It is concluded that birth hypoxia augments plasma testosterone during the critical period of the neonatal testosterone surge, by a mechanism that is independent of NMDA-mediated LH secretion, but may involve increased circulating ACTH.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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“…with the reduction in hepatic 5a-reductase expression in PNS male rats, 5a-reductase mRNA expression in the brains of fetal, prepubertal and adult PNS rats is downregulated (Ordyan & Pivina 2005, Paris et al 2011. In the brain, 5a-reductase generates neurosteroids such as allopregnanolone (3a-hydroxy-5a-pregnan-20-one) and androstanediol (5a-androstane-3b,17b-diol), which have anxiolytic and stress-reducing actions (Bitran et al 1995, Patchev et al 1996, Edinger & Frye 2004, Brunton et al 2009, Handa et al 2009).…”

Section: Figurementioning

confidence: 99%

Sex-specific effects of prenatal stress on glucose homoeostasis and peripheral metabolism in rats

Brunton¹,

Sullivan²,

Kerrigan³

et al. 2013

Journal of Endocrinology

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Glucocorticoid overexposure during pregnancy programmes offspring physiology and predisposes to later disease. However, any impact of ethologically relevant maternal stress is less clear, yet of physiological importance. Here, we investigated in rats the short-and longterm effects in adult offspring of repeated social stress (exposure to an aggressive lactating female) during late pregnancy on glucose regulation following stress, glucose-insulin homoeostasis and peripheral expression of genes important in regulating glucose and lipid metabolism and glucocorticoid action. Prenatal stress (PNS) was associated with reduced birth weight in female, but not male, offspring. The increase in blood glucose with restraint was exaggerated in adult PNS males compared with controls, but not in females. Oral glucose tolerance testing showed no effects on plasma glucose or insulin concentrations in either sex at 3 months; however, at 6 months, PNS females were hyperinsulinaemic following an oral glucose load. In PNS males, plasma triglyceride concentrations were increased, with reduced hepatic mRNA expression of 5a-reductase and peroxisome proliferator-activated receptor a (Ppara (Ppara)) and a strong trend towards reduced peroxisome proliferatoractivated receptor gamma coactivator 1a (Pgc1a (Ppargc1a)) and Pparg (Pparg) expression, whereas only Pgc1a mRNA was affected in PNS females. Conversely, in subcutaneous fat, PNS reduced mRNA expression of 11b-hydroxysteroid dehydrogenase type 1 (11bhsd1), phosphoenolpyruvate carboxykinase (Pepck (Pck1)), adipose triglyceride lipase (Atgl) and diglyceride acyltransferase 2 (Dgat2) in females, but only Pepck mRNA expression was reduced in PNS males. Thus, prenatal social stress differentially programmes glucose homoeostasis and peripheral metabolism in male and female offspring. These long-term alterations in physiology may increase susceptibility to metabolic disease.Key Words " 5a-reductase " adipose " corticosterone metabolism " early life stress " liver " sex difference

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“…The role of stressors for regulating 5α-reductase and other steroidogenic enzymes, and their neurosteroid products, throughout development has been described. Prenatal immobilization stress on gestational days 15–18 is associated with initial decreases in 5α-reductase activity in the cerebral cortex and hypothalamus of PND 1 male pups, but elevated 5α-reductase activity in the cortex, hippocampus, and hypothalamus on PND 5 (Ordyan and Pivina, 2005). Another model of early life stress, isolation rearing, for 5–8 weeks reduces expression of 5α-reductase and levels of 3α,5α-THP in the nucleus accumbens and medial prefontal cortex of male rats (Bortolato et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Gestational or acute restraint in adulthood reduces levels of 5α-reduced testosterone metabolites in the hippocampus and produces behavioral inhibition of adult male rats

Walf¹,

Frye²

2012

Front. Cell. Neurosci.

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Stressors, during early life or adulthood, can alter steroid-sensitive behaviors, such as exploration, anxiety, and/or cognitive processes. We investigated if exposure to acute stressors in adulthood may alter behavioral and neuroendocrine responses of male rats that were exposed to gestational stress or not. We hypothesized that rats exposed to gestational and acute stress may show behavioral inhibition, increased corticosterone, and altered androgen levels in the hippocampus. Subjects were adult, male offspring of rat dams that were restrained daily on gestational days 14–20, or did not experience this manipulation. Immediately before testing, rats were restraint stressed for 20 min or not. During week 1, rats were tested in a battery of tasks, including the open field, elevated plus maze, social interaction, tailflick, pawlick, and defensive burying tasks. During week 2, rats were trained and tested 24 h later in the inhibitory avoidance task. Plasma corticosterone and androgen levels, and hippocampal androgen levels, were measured in all subjects. Gestational and acute restraint stress increased plasma levels of corticosterone, and reduced levels of testosterone's 5α-reduced metabolites, dihydrotestosterone (DHT) and 3α-androstanediol (3α-diol), but not the aromatized metabolite, estradiol (E2), in plasma or the hippocampus. Gestational and acute restraint stress reduced central entries made in the open field, and latencies to enter the shock-associated side of the inhibitory avoidance chamber during testing. Gestational stress reduced time spent interacting with a conspecific. These data suggest that gestational and acute restraint stress can have actions to produce behavioral inhibition coincident with increased corticosterone and decreased 5α-reduced androgens of adult male rats. Thus, gestational stress altered neural circuits involved in the neuroendocrine response to acute stress in early adulthood.

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Effects of Prenatal Stress on the Activity of an Enzyme Involved in Neurosteroid Synthesis During the “Critical Period” of Sexual Differentiation of the Brain in Male Rats

Cited by 17 publications

References 24 publications

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Sex-specific effects of prenatal stress on glucose homoeostasis and peripheral metabolism in rats

Gestational or acute restraint in adulthood reduces levels of 5α-reduced testosterone metabolites in the hippocampus and produces behavioral inhibition of adult male rats

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