The Effects of Prenatal Alcohol Exposure on the Behavior of Rats During Their Life Span

Abstract

Ontogenesis is closely related to the ability to adapt to endogenous and exogenous stimuli. However, this precondition for viability does not remain stable; it changes in correlation to the phases of life. In this long-term study with rats, the extent to which moderate prenatal damage influences the adaptability in the juvenile, adult and senile phases was examined. For this purpose rat fetuses were exposed to alcohol (6 g/kg bw/day) by treating the pregnant rats via drinking water from gestation days 7 to 17. In the juvenile phase (0-3 months), no substantial differences in comparison to controls were recorded. Exceptions were a delayed development in the negative geotaxis (posture reflex) and a transiently higher exploratory activity in the open field test. In the adult phase (> 3-27 months), reduced performance was observed in basic functions such as body temperature regulation. Additionally, diminished performance was seen in response to high demands in motor-coordination (rotorod). During the senile phase (> 27 months), impairment of nearly all tested functions occurred earlier and was more pronounced.

Prenatal choline supplementation mitigates the adverse effects of prenatal alcohol exposure on development in rats

“…To our knowledge, this is the first report of changes in physical maturation associated with prenatal choline supplementation. Similar to previous reports, prenatal alcohol exposure also delayed righting reflex [24,56,62], negative geotaxis [27,36], grip strength [27], and motor coordination. In contrast, prenatal alcohol advanced and enhanced cliff avoidance.…”

Prenatal ethanol exposure in rats alters serotonergic-mediated behavioral and physiological function

“…Ethanol-exposed animals show behavioral and physiological changes consistent with altered 5-HT function. For example, ethanol-exposed animals show response perseveration (Riley et al 1979), increased anxiety (Osborn et al 1998) and aggression (Kršiak et al 1977), decreased thermoregulatory ability (Jänicke and Coper 1993), altered sexual behavior, increased acoustic startle responses (Potter and Berntson 1987), and increased locomotor activity (Kaneko et al 1993). However, these experiments focused primarily on young animals, with less consideration of the long-term effects in adult animals.…”

Auditory Brainstem Response (ABR) Abnormalities Across the Life Span of Rats Prenatally Exposed to Alcohol

“…A few animal studies on prenatal alcohol exposure have explored long‐term effects. These studies found shortened life span in adult rats (Abel et al., 1987), reduced somatosensory cortex whisker vibrissae barrel field size in 7‐month‐old adult rats (Chappell et al., 2007), altered behavior in aged rats (Abel and Berman, 1994; Abel and Dintcheff, 1986; Janicke and Coper, 1993; Markel et al., 1995), enhanced memory loss in aged mice (Dumas and Rabe, 1994), altered hypothalamic–pituitary–adrenal (HPA) axis function and depression/anxiety disorders in adult rodents (Weinberg et al., 2008), diabetes in adult rats (Pennington et al., 2002; Yao et al., 2006), and preliminary evidence of abnormal auditory function in rats aged 6 to 18 months (Church et al., 1996). Lifelong effects are of interest because the Barker hypothesis states that an adverse prenatal environment can program the embryo or fetus for adult‐onset diseases, such as coronary heart disease, hypertension, type II diabetes, enhanced age‐related neural degeneration, depression/anxiety and other psychiatric disorders, and a shortened life span (Barker, 2004).…”

“…We hypothesized that animals prenatally exposed to alcohol would exhibit ABR evidence of hearing loss, impaired neural responsivity to a stimulus stressor, prolonged neural transmission times, and enhanced age‐related neural degeneration. Based on prior longevity studies of prenatal toxicity, we predicted that ABR abnormalities would show an age‐related pattern characterized by strong effects in pre‐adolescence, which would largely dissipate in young adulthood and then recur in middle‐aged adulthood (Barone et al., 1995; Church et al., 2010; Dumas and Rabe, 1994; Janicke and Coper, 1993, 1994; Markel et al., 1995; Martin, 1986; Schallert, 1983; Wallace et al., 1972). We also predicted reduced body weights and a shortened life span as consequences of prenatal alcohol exposure (Abel et al., 1987; Church et al., 2004b, 2010).…”