Development of sexual behavior in prenatally ethanol-exposed rats

Hård, Ernest; Dahlgren, I.Lena; Engel, Jörgen A.; Larsson, Knut; Liljequist, Sture; Lindh, Ann-Sofie; Musi, Barbara

doi:10.1016/0376-8716(84)90019-x

Cited by 67 publications

(25 citation statements)

References 29 publications

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“…It is possible that the organizational effects of androgen were attenuated in PAE, and altered in PS fetuses such that marginally opposite effects were observed. Interestingly, male offspring of rats prenatally exposed to alcohol or stress were reported to display atypical sexual behaviors, such as an increased potential for lordosis, which indicates a failure of masculinization in adulthood (Ward, 1972; Hard et al, 1984; Ward et al, 1994). It is possible that the altered MR and GR expression observed in PAE and PS fetuses sets the stage for further changes in HPA function and altered adrenal-gonadal interactions throughout development and into adulthood.…”

Section: Discussionmentioning

confidence: 99%

Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

Chiu

Ellis

et al. 2017

Neuroscience

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Adverse intrauterine environments increase vulnerability to chronic diseases across the lifespan. The hypothalamic-pituitary-adrenal (HPA) axis, which integrates multiple neuronal signals and ultimately controls the response to stressors, may provide a final common pathway linking early adversity and adult disease. Both prenatal alcohol exposure (PAE) and prenatal stress (PS) induce a hyperresponsive HPA phenotype in adulthood. As glucocorticoids are pivotal for the normal development of many fetal tissues including the brain, we used animal models of PAE and PS to investigate possible mechanisms underlying fetal programming of glucocorticoid signaling in the placenta and fetal brain at gestation day (GD) 21. We found that both PAE and PS dams had higher corticosterone levels than control dams. However, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) enzyme levels were increased in PAE and unchanged in PS placentae, although there were no differences in 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) levels. Moreover, only PAE fetuses showed decreased body weight and increased placental weight, and hence a lower fetal/placental weight ratio, a marker of placenta efficiency, compared to all other prenatal groups. Importantly, PAE and PS differentially altered corticosteroid receptor levels in placentae and brains. In the PS condition, maternal corticosterone was negatively correlated with both 11β-HSD1 and mineralocorticoid receptor (MR) proteins levels in male and female placentae, whereas in the PAE condition, there were trends for a positive correlation between maternal corticosterone and 11β-HSD1, regardless of sex, and a negative correlation between maternal alcohol intake and MR in male placentae. In fetal brains, sexually dimorphic changes in MR and glucocorticoid receptor (GR) levels, and the MR/GR ratio seen in C fetuses were absent in PAE and PS fetuses. In addition, PS but not PAE female fetuses had higher MR and lower GR expression levels in certain limbic areas compared to C female fetuses. Thus the similar adult HPA hyperresponsive phenotype in PAE and PS animals likely occurs through differential effects on glucocorticoid signaling in the placenta and fetal brain.

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Section: Discussionmentioning

confidence: 99%

Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

Chiu

Ellis

et al. 2017

Neuroscience

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“…While Hard et al [13] found no differences in age for vaginal opening between ethanol-exposed and control rats, the methodology and design of their experiment was differ ent and nutritional controls were not included. However, Boggan et al [2] also reported a delay in sexual maturation in PEA mice only during the period of organogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…1,18,[22][23][24][25]. Various female abnormalities have also been reported, such as genital anomalies in girls diagnosed with the fetal alcohol syn drome (FAS) [12], interference in the normal course of sex ual differentiation [13,16] and delay in puberty [1], The mechanism(s) of these alterations is unknown.Several studies have demonstrated that chronic and acute ethanol intakes have a negative effect on the hypothalamic-pituitary-gonadal axis in adult mammals including man [for reviews, see ref. 5, 17,29,30,32].…”

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confidence: 99%

Effect of Prenatal Alcohol Exposure on Sexual Maturation of Female Rat Offspring

Esquifino

Sanchis²,

Guerri³

1986

Neuroendocrinology

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To assess sexual maturation of female offspring from alcoholic rats, vaginal opening, body weight, prolactin (PRL), luteinizing hormone (LH) and growth hormone (GH) were followed during development. The vaginal opening in the female offspring from alcohol-fed dams was delayed compared with the offspring from both pair-fed and normally fed dams. There was an increase in plasma PRL levels together with a decrease in levels of plasma LH at the time of the opening of the vagina in rats prenatally exposed to alcohol (PEA) with respect to both control groups. The increase in PRL was the only hormonal alteration which persisted into adulthood (120 days). In general, there were no changes in levels of plasma GH between experimental and control groups. These data indicate that PEA results in a modification in secretions of PRL and LH as well as in a delay in the opening of the vagina.

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“…For example, the change in testosterone levels may contribute to the female-like juvenile play [37] and active social interactions [32], the feminized patterns of social partner preference [38], and the decrease in the ano-genital distance [10] seen in ethanol-exposed males. Ethanol-exposed males are more likely to exhibit lordosis behavior [39] and are less likely to ejaculate [9]. 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].…”

Section: Discussionmentioning

confidence: 57%

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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Development of sexual behavior in prenatally ethanol-exposed rats

Cited by 67 publications

References 29 publications

Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

Effect of Prenatal Alcohol Exposure on Sexual Maturation of Female Rat Offspring

Ethanol exposure during development reduces resident aggression and testosterone in rats

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