Loss of Reproductive Competence at an Earlier Age in Female Rats Exposed Prenatally to Ethanol

Abstract

Previous studies have shown that prenatal ethanol exposure can partially masculinize or defeminize neurobehavioral development of female rats. An early age of onset of anovulation is one of the primary characteristics of partial defeminization. Consequently, we examined the occurrence of anovulation in fetal alcohol-exposed (FAE) female rats at 2, 6, and 12 months of age using both vaginal cytology as well as wheel-running behavior. We assessed the ability of estrogen and progesterone to elicit proprioceptive behaviors and lordosis at 2 and 17 months of age. Female subjects were derived from Sprague-Dawley dams administered an ethanol liquid diet (35% ethanol-derived calories), a pair-fed isocaloric liquid diet, or fed lab chow from days 14 to 22 of gestation. Litter representatives were placed in a computer-monitored wheel-running apparatus under a 12-hr lighting schedule from 49 to 60 days of age. Vaginal smears were taken from littermates during this same period. This same procedure was conducted again from 180 to 196 and from 380 to 396 days of age, except that vaginal cytology was examined in the same animals immediately after wheel-running behavior was studied. At approximately 2 months of age, a normal cyclical pattern of wheel-running, characteristic of 4- to 5-day estrus cycles, was observed in all animals. No differences were detected in mean activity levels during the wheel-running period. This was accompanied by normal cyclic vaginal cytology and normal proprioceptive behaviors and lordosis. At 6 months of age, FAE females exhibited significantly reduced wheel-running.(ABSTRACT TRUNCATED AT 250 WORDS)

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

“…It has been argued that cognitive and behavioral abnormalities produced by prenatal ethanol exposure may be masked in young-adult animals because of compensatory mechanisms or strategies, but that these compensatory mechanisms may break down due to stressful situations, complex testing procedures, or aging (Riley, 1990). Of particular relevance to the performance of mid-aged E animals in the present study, previous research has shown that E animals exhibit behavioral and hormonal hyperactivity to stress (Angelogianni & Gianoulakis, 1989;Nelson et al, 1986;Osborne et al, 1980;Taylor et al, 1982;Weinberg, 1988Weinberg, , 1992Weinberg, , 1993 as well as accelerated aging, including a shortened life span (Abel et al, 1987) and an earlier loss of reproductive function in E female rats (McGivern et al, 1995). These factors were expected to affect spatial learning and memory negatively in mid-aged E animals.…”

“…Therefore, not only may impaired performance on spatial learning and memory tasks in E animals be related to stress-induced performance deficits associated with increased HPA activity but aging E animals also may experience an accelerated rate of impairment in hippocampal-mediated functions. Although this remains to be investigated, research demonstrating accelerated aging in E animals, including a shortened lifespan in E animals (Abel, Church, & Dintcheff, 1987) and an earlier loss of reproductive function in E female rats (McGivern, McGeary, Robeck, Cohen, & Handa, 1995), alludes to the possibility that E animals may experience an increased rate of aging for physiological functions.…”

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

“…The reason(s) for these sexually dimorphic changes is unclear, but it is possible that these behavioral patterns may be related to females reaching hormonal and physical markers of puberty prior to males [60]. Prenatal ethanol exposure may shift the onset of these developmental stages and thereby alter sex-hormones and brain development [61, 62]. …”

Neuronal basis of reproductive dysfunctions associated with diet and alcohol: From the womb to adulthood

“…Our unpublished data also indicated that PAE females: (1) did not show an increase in E 2 levels as a function of age, resulting in lower E 2 levels relative to control females; (2) demonstrated a lag in the age-related increase of P 4 levels observed in controls; (3) failed to show a similar increase in PRL and LH levels as a function of age as reported in controls; and (4) had lower levels of PRL and LH (Sliwowska et al, unpublished data). These alterations may in turn lead to early incidence of acyclicity, an indication of premature reproductive aging [78]. As hormone levels fluctuate during the day, it is worth noting that blood was collected between 9:00 and 12:00 h. Thus, together with delayed onset of puberty, the reproductive window -at least in animal models of PAE -may be shorter.…”