Postparturitional Testosterone Surge in Male Offspring of Rats Stressed and/or Fed Ethanol during Late Pregnancy

Ward, O. Byron; Ward, Ingeborg L.; Denning, John H.; French, Jeffrey A.; Hendricks, Shelton E.

doi:10.1006/hbeh.2001.1746

Cited by 34 publications

(30 citation statements)

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“…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%

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: Introductionmentioning

confidence: 99%

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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“…Ward and colleagues [11,12,41] have repeatedly shown that the effects of prenatal ethanol exposure often synergize with prenatal stress to affect measures of male sexual behavior and reduce testosterone levels during development. In particular, they found that while prenatal stress suppresses prenatal and does not affect postnatal testosterone, ethanol exposure enhances prenatal and suppresses postnatal testosterone levels [11,12,41].…”

Section: Discussionmentioning

confidence: 99%

“…In particular, they found that while prenatal stress suppresses prenatal and does not affect postnatal testosterone, ethanol exposure enhances prenatal and suppresses postnatal testosterone levels [11,12,41]. Prenatal exposure to ethanol and stress combined have the most dramatic feminizing effect on male sexual behavior [9].…”

Section: Discussionmentioning

confidence: 99%

“…Ethanol exposure from GD 12 to PD 10 decreases testosterone in male rats on PD 55 and PD 110 [10]. Ethanol exposure from GD 10 to 19 augments testosterone levels in male rats on GD 18 and 19 [11] and suppresses it during the early postnatal period [12]. Low levels of testosterone during development and/ or during adulthood have been shown to result in low levels of offensive inter-male aggression in rats and mice [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…The decrease in masculinization may also be responsible for the decrease in aggression behavior seen in the current study, since female rats typically show low levels of aggression [14,40]. Nevertheless, in order to begin to understand the mechanism of the ethanol-induced reduction in adult testosterone levels, a developmental time course describing the changes in testosterone over the lifespan is necessary.Ward and colleagues [11,12,41] have repeatedly shown that the effects of prenatal ethanol exposure often synergize with prenatal stress to affect measures of male sexual behavior and reduce testosterone levels during development. In particular, they found that while prenatal stress suppresses prenatal and does not affect postnatal testosterone, ethanol exposure enhances prenatal and suppresses postnatal testosterone levels [11,12,41].…”

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Ethanol exposure during development reduces resident aggression and testosterone in rats

Lugo

Marino

Gass

et al. 2006

Physiology & Behavior

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Ethanol exposure during development has been shown to alter social behaviors in people, but the range of deficits is not clear. Using an animal model of Fetal Alcohol Spectrum Disorders, intermale aggression and testosterone levels were examined in adult rats. Rats were exposed to ethanol during the entire prenatal period and from postnatal day 2 through 10. Ethanol was administered via intragastric intubation. Two other groups consisted of a nontreated control and an intubated control group that was exposed to the administration procedures but not ethanol. Both offensive and defensive aggression were examined in experimental residents and intruders under three different housing conditions for the resident males: (1) with another male, (2) with a pregnant female, and (3) with a female and litter fathered by the experimental animal. When housed with a female and litter, ethanol-exposed rats displayed reduced offensive aggression compared to control groups under the same condition. Defensive aggression in the non-experimental intruders was reduced in this same condition. There were no differences in duration of non-aggressive social behaviors among the groups in any of the housing conditions. Testosterone levels were reduced in ethanol-exposed rats compared to controls. In summary, ethanol exposure over the combined prenatal and postnatal periods reduces aggressive behavior in a condition where aggressive behavior is normally seen. This reduction may be related to lower testosterone levels. KeywordsFetal alcohol syndrome; Aggression; Resident-intruder paradigm; Social behavior; Prenatal alcohol Fetal Alcohol Spectrum Disorders (FASD) describes those individuals who manifest mild to severe disturbances of physical, behavioral, emotional, and/or social functioning due to in utero ethanol exposure. FASD individuals are found to commit high rate of crimes against others, engage in inappropriate sexual behavior, and are described as having a failure to consider the consequences of their actions [1,2]. Even though FASD individuals show high rates of crime, no direct measures of aggressive behaviors or testosterone in FAS individuals have been conducted. [3][4][5][6]; ethanol exposure from gestation day (GD) 6 to 19 increases offensive aggression in rats [7]. Ethanol exposure during the last four days of pregnancy and from postnatal day (PD) 1 to PD 4 increases aggression, while ethanol exposure confined to the period from PD 1 to 4 did not affect aggressive behavior in mice [8]. However, another study found that ethanol exposure from birth until PD 14 decreases aggression in mice [6]. These studies suggest that prenatal ethanol exposure may increase aggression, while postnatal ethanol exposure may decrease aggression. However, many of the early studies used ethanol administration procedures that were confounded by nutritional effects [4][5][6]8] or resulted in minimal transfer of ethanol to the pup [6]. The effect of ethanol exposure during the entire gestation period and during early postnatal development (i.e...

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Effects of restraint stress in gestation: Implications for rodent developmental toxicology studies

Golub

Campbell

Kaufman

et al. 2004

Birth Defects Research Pt B

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Restraint has been used as a procedure to study the effects of stress on gestation outcome in rodents. The effects of restraint could potentially be used as a model for the impact of general stress produced by high doses of toxicants and other interventions. In mice, restraint in the peri-implantation period leads to implantation failure, and restraint at appropriate times in organogenesis produces cleft palate, supernumerary ribs, and resorption. In rats, there is some evidence for an association with restraint for implantation failure, but not for the morphological anomalies. Restraint in late gestation alters adult sexual behavior of male rat offspring, but consequences for their fertility are not known. Intrauterine growth retardation is not commonly associated with gestational restraint. In the few studies where they have been directly compared, different restraint procedures produced graded, qualitatively different, or no effects. Adrenocortical hormones have been implicated as mediating the effect of restraint on cleft palate, but not on supernumerary ribs, implantation failure, or sexual differentiation. Given the variety of restraint procedures and the varying species-dependent consequences, it is not possible to infer a generalizable pattern of developmental effects due to gestational stress from the restraint literature. As an alternative approach, contemporary methods in gene expression and developmental biology could profitably be applied to understanding different patterns of stress-mediated effects of toxicant exposures on intrauterine development. Birth Defects Res B 71:26-36, 2004. r 2004 Wiley-Liss, Inc.

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Postparturitional Testosterone Surge in Male Offspring of Rats Stressed and/or Fed Ethanol during Late Pregnancy

Cited by 34 publications

References 37 publications

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Ethanol exposure during development reduces resident aggression and testosterone in rats

Effects of restraint stress in gestation: Implications for rodent developmental toxicology studies

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