Academic journal article Cognitive, Affective and Behavioral Neuroscience

Maternal Supplementation of Nucleotides Improves the Behavioral Development of Prenatal Ethanol-Exposed Mice

Academic journal article Cognitive, Affective and Behavioral Neuroscience

Maternal Supplementation of Nucleotides Improves the Behavioral Development of Prenatal Ethanol-Exposed Mice

Article excerpt

Published online: 22 October 2013

© Psychonomic Society, Inc. 2013

Abstract Maternal ethanol consumption during pregnancy can induce learning deficits in the offspring. The objective of this study was to assess whether supplementation of exogenous nucleotides during pregnancy and lactation would ameliorate prenatal ethanol-induced learning and memory deficits in the offspring of mice, and to explore the possible mechanisms. In the present study, pregnant C57BL/6J mice were exposed to ethanol (5 g/kg body weight) intragastrically from gestational day (GD) 6 to GD15. The dams in exogenous nucleotide intervention groups were fed with feed containing 0.01 %, 0.04 %, or 0.16 % nucleotide powder, with control and ethanol groups receiving normal feed. The dams were allowed to deliver naturally and to breast feed their offspring. After weaning, behavioral tests were carried out in the offspring of each group. Serum oxidation indexes were analyzed, and the hippocampus of each offspring was collected and detected for acetyl cholinesterase (AChE) activity and the expression of p-CREB, CREB, and BDNF. The results showed that maternal supplementation with exogenous nucleotides during pregnancy could ameliorate prenatal ethanol-induced learning and memory deficits in the offspring of mice, through improving their antioxidant capacity, reversing hippocampus AChE levels, and allowing the expression of some proteins related to learning and memory. However, different sensitivities were found between the two sexes.

Keywords Nucleotide · Ethanol · Learning and memory deficits · Intervention

Prenatal ethanol exposure is one of the main risk factors that result in a series of birth defects and developmental retardation, the most serious of which is termed fetal alcohol syndrome (FAS) (Detering, Reed, Ozand, & Karahasan, 1979; Ouellette, Rosett, Rosman, & Weiner, 1977; Welch-Carre, 2005). FAS patients often have more than one neurodevelopmental disorder that have far-reaching impacts on human life, including substantial, lifelong impairments in intellectual, cognitive, and psychosocial functioning. Although it is well known that alcoholic beverage drinking during gestation may jeopardize the offspring, the prevalence of FAS is still increasing worldwide. Especially in some developing countries where the social status of women is improving and females are attending more social activities than ever before, the odds of unintentional drinking during early pregnancy (the first trimester, when many women may not be aware of their pregnancy) are increasing rapidly.

Not only does the disease cause heavy psychological pressure to families, it also brings heavy economic burdens to both families and governments. In Canada, the total adjusted annual costs associated with FAS were estimated at $14,342 per child (Naha, Lee, Naser, Park, Kim, & Kim, 2009); in the US, estimates of the annual economic impact of FAS reached up to $9.7 billion (Yeaney, He, Tang, Malouf, O'Riordan, Lemmon, & Bearer, 2009), and it would cost $2, 342 per year to prevent one case of FAS (Goodlett & Horn, 2001). Considering the great loss and cost that we have to sacrifice, it is of great significance to find measures to ameliorate the detrimental effects of prenatal ethanol exposure.

Our previous research showed that 5.0 g/kg body weight ethanol consumption during the organogenesis period in mice could jeopardize the development of the fetal central nervous system, causing excessive cell apoptosis, decreased adenosine 5?-triphosphate content in the fetal brain, and microcephaly (Xu, Liu, & Li, 2005), and could also cause fetal brain proteomic changes (Xu, Tang, & Li, 2008). Meanwhile, maternal supplementation with one-carbon unit, which are necessary materials for the de novo synthesis of nucleic acid, can improve ethanol-induced developmental toxicity in mouse fetuses (Xu et al., 2008). Considering the limitation of de novo synthesis of nucleic acid under stress conditions- such as impaired immunity, liver injury, and rapid growth periods (Kvigne, Leonardson, Neff-Smith, Brock, Borzelleca, & Welty, 2004) - we hypothesized that enhancement of the salvage pathway of nucleic acid production by supplementing exogenous nucleotides might be an effective and economical way to reverse prenatal ethanol-induced learning and memory deficits. …

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