Prenatal dexamethasone or stress but not ACTH or corticosterone alter sexual behavior in male rats

Holson, R.Robert; Gough, B.; Sullivan, Patricia A.; Badger, Thomas M.; Sheehan, Daniel M.

doi:10.1016/0892-0362(94)00074-n

Cited by 116 publications

(83 citation statements)

References 69 publications

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“…Similarly, prolonged prenatal stress and the associated release of endogenous maternal glucocorticoids are known to feminize behavioral responses in male rats (Holson et al, 1995;Ward, 1972). Our results, however, indicate that effects involve both sexes and occur at a lower threshold than for persistent growth deficits.…”

Section: Discussioncontrasting

confidence: 54%

“…Earlier studies identified effects on behavior and hypothalamo-pituitary-adrenal axis function in male offspring after developmental exposure to higher doses or longer durations of glucocorticoid treatment, regimens that elicit persistent growth retardation (Dean et al, 2001;Holson et al, 1995;Machhor et al, 2004). Similarly, prolonged prenatal stress and the associated release of endogenous maternal glucocorticoids are known to feminize behavioral responses in male rats (Holson et al, 1995;Ward, 1972).…”

Section: Discussionmentioning

confidence: 99%

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Gestational Dexamethasone Treatment Elicits Sex-Dependent Alterations in Locomotor Activity, Reward-Based Memory and Hippocampal Cholinergic Function in Adolescent and Adult Rats

Kreider

Levin

Seidler

et al. 2005

Neuropsychopharmacol

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Glucocorticoids are the consensus treatment for preventing respiratory distress syndrome in preterm infants but there is emerging evidence of subsequent neurobehavioral abnormalities, independent of somatic growth effects. Pregnant rats were given 0.2 mg/kg of dexamethasone, a dose commensurate with clinical use, on gestational days 17-19 and behavioral evaluations were made on the offspring in adolescence and adulthood. The dexamethasone groups had the same body weights as the controls but nevertheless displayed long-term, sex-selective alterations in locomotor and cognitive behaviors. In the figure-8 activity apparatus, dexamethasone treatment ablated the normal sex differences in locomotor activity by reducing values in females to the lower level typical of males; habituation of activity similarly was impaired in females, reducing the profile to match that of control males, while male rats in the dexamethasone group showed a partially feminized pattern of habituation. In the 8-arm radial maze, control rats displayed typical sex differences, with male rats performing more accurately than females. Dexamethasone treatment eliminated this normal dichotomy, delaying learning in males while improving performance in females to the level normally seen in control males. Finally, we assessed hippocampal [3 H]hemicholinium-3 binding as a biomarker for cholinergic synaptic activity, and again found loss of sex differences in the dexamethasone group: values in males were increased to the higher levels typical of females. These results indicate that gestational treatment with dexamethasone obtunds the normal sex differences in neurochemistry and behavior that are typically seen in adolescence in adulthood, thus producing sex-selective alterations in activity, learning, and memory.

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Section: Discussioncontrasting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Gestational Dexamethasone Treatment Elicits Sex-Dependent Alterations in Locomotor Activity, Reward-Based Memory and Hippocampal Cholinergic Function in Adolescent and Adult Rats

Kreider

Levin

Seidler

et al. 2005

Neuropsychopharmacol

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“…Together, these data suggest that perinatal GC treatment interferes with the sexual differentiation of the SNc and VTA cytoarchitecture and, in particular, results in a feminization or demasculinization in the male. Notably, prenatal exposure to dexamethasone or stress (which would increase endogenous adrenal steroids) have been reported to demasculinize or feminize reproductive behaviors in adult male rats (Ward, 1972;Holson et al, 1995). Recent studies have also shown that prenatal dexamethasone treatment eliminated sex differences in locomotor and cognitive behaviors by distinct and often opposite effects in males and females (Kreider et al, 2005).…”

Section: Gc Programming Of Midbrain Da Cytoarchitecturementioning

confidence: 99%

The Size and Distribution of Midbrain Dopaminergic Populations are Permanently Altered by Perinatal Glucocorticoid Exposure in a Sex- Region- and Time-Specific Manner

McArthur

McHale

Gillies

2006

Neuropsychopharmacol

110

106

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Central dopaminergic (DA) systems appear to be particularly vulnerable to disruption by exposure to stressors in early life, but the underlying mechanisms are poorly understood. As endogenous glucocorticoids (GCs) are implicated in other aspects of neurobiological programming, this study aimed to characterize the effects of perinatal GC exposure on the cytoarchitecture of DA populations in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). Dexamethasone was administered non-invasively to rat pups via the mothers' drinking water during embryonic days 16-19 or postnatal days 1-7, with a total oral intake circa 0.075 or 0.15 mg/ kg/day, respectively; controls received normal drinking water. Analysis of tyrosine hydroxylase-immunoreactive cell counts and regional volumes in adult offspring identified notable sex differences in the shape and volume of the SNc and VTA, as well as the topographical organization and size of the DA populations. Perinatal GC treatments increased the DA population size and altered the shape of the SNc and VTA as well as the organization of the DA neurons by expanding and/or shifting them in a caudal direction. This response was sexually dimorphic and included a feminization or demasculinization of the three-dimensional cytoarchitecture in males, and subtle differences that were dependent on the window of exposure. These findings demonstrate that inappropriate perinatal exposure to GCs have enduring effects on the organization of midbrain DA systems that are critically important for normal brain function throughout life.

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“…In rodents, prenatal stress is associated with negative pregnancy outcomes such as low birth weight, reduced litter sizes and lower survival rates (de Catanzaro 1988, Pratt & Lisk 1991, Brunton & Russell 2010, and in the adult offspring, it is associated with heightened anxiety (Fride & Weinstock 1988, Vallee et al 1997, Fan et al 2009, Brunton & Russell 2010, enhanced or prolonged hypothalamo-pituitary-adrenal (HPA) axis (Fig. 1) responses to acute stress (Takahashi & Kalin 1991, Weinstock et al 1992, McCormick et al 1995, Koenig et al 2005, Fan et al 2009, Brunton & Russell 2010, hypertension (Igosheva et al 2004), impaired glucose homoeostasis (Brunton et al 2013), insulin resistance (Nilsson et al 2001), diet-induced obesity (Nilsson et al 2001, Tamashiro et al 2009), impaired neural development (Lemaire et al 2000), cognitive deficits (Lemaire et al 2000, and abnormal social (Patin et al 2005, Lee et al 2007 and reproductive behaviours (Holson et al 1995, Frye & Orecki 2002.…”

Section: Introductionmentioning

confidence: 99%

Effects of maternal exposure to social stress during pregnancy: consequences for mother and offspring

2013

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A suboptimal in utero environment, for example, as a result of maternal stress, can have detrimental effects on the pregnancy and long-term adverse 'programming' effects on the offspring. This article focuses on the effects of prenatal social stress on the mother, her pregnancy and the offspring, since these issues have ethological relevance in both animals and humans. The consequences of social stress exposure depend on when during pregnancy the stress occurs, and many of the effects on the offspring are sex specific. Social stress during early pregnancy tends to result in pregnancy loss, whereas stress exposure later in pregnancy, when the mother has already invested considerable resources in the foetuses, results in programmed offspring of low birth weight: a risk factor for various adulthood diseases. Neuroendocrine and behavioural responses to stress in the offspring are particularly sensitive to foetal programming by prenatal stress, indicated by enhanced hypothalamo-pituitary-adrenal (HPA) axis responses and increased anxiety behaviour, which result from permanent changes in the offspring's brain. The dysregulation of HPA axis function may also interfere with other systems, for example, the hypothalamic-pituitary-gonadal axis, as there is evidence for alterations in steroidogenesis, reproductive potential and impaired reproductive/social behaviours in prenatally stressed offspring. Prenatal social stress also programmes future maternal behaviour, highlighting the potential for negative phenotypes to be transmitted to future generations. The possible mechanisms through which maternal stress during pregnancy is transmitted to the foetuses and the foetal brain is programmed by prenatal stress and the potential to overwrite programming of the offspring are discussed.Reproduction (2013) 146 R175-R189

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Prenatal dexamethasone or stress but not ACTH or corticosterone alter sexual behavior in male rats

Cited by 116 publications

References 69 publications

Gestational Dexamethasone Treatment Elicits Sex-Dependent Alterations in Locomotor Activity, Reward-Based Memory and Hippocampal Cholinergic Function in Adolescent and Adult Rats

Gestational Dexamethasone Treatment Elicits Sex-Dependent Alterations in Locomotor Activity, Reward-Based Memory and Hippocampal Cholinergic Function in Adolescent and Adult Rats

The Size and Distribution of Midbrain Dopaminergic Populations are Permanently Altered by Perinatal Glucocorticoid Exposure in a Sex- Region- and Time-Specific Manner

Effects of maternal exposure to social stress during pregnancy: consequences for mother and offspring

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