51. Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise.
- Author
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Redila VA, Olson AK, Swann SE, Mohades G, Webber AJ, Weinberg J, and Christie BR
- Subjects
- Alcohol-Induced Disorders, Nervous System pathology, Animals, Atrophy chemically induced, Atrophy physiopathology, Atrophy therapy, Cell Division drug effects, Cell Division physiology, Disease Models, Animal, Down-Regulation drug effects, Down-Regulation physiology, Female, Male, Neuronal Plasticity drug effects, Neuronal Plasticity physiology, Neurons drug effects, Neurons physiology, Pregnancy, Prenatal Exposure Delayed Effects pathology, Rats, Rats, Sprague-Dawley, Stem Cells drug effects, Stem Cells physiology, Up-Regulation physiology, Alcohol-Induced Disorders, Nervous System physiopathology, Cell Proliferation drug effects, Hippocampus drug effects, Hippocampus physiopathology, Motor Activity physiology, Prenatal Exposure Delayed Effects physiopathology
- Abstract
The ingestion of ethanol during pregnancy has a number of deleterious consequences for the unborn offspring, producing structural and functional deficits that affect the brain and many other organs into adulthood. The hippocampus is a brain area that is particularly sensitive to ethanol's adverse effects. In a previous study we showed that voluntary exercise can ameliorate deficits in long-term potentiation and behavior that occur following prenatal ethanol exposure (Eur J Neurosci, 2005, 21, 1719-1726). In the present study, we investigated the effects of prenatal ethanol exposure on neurogenesis in adulthood, and tested the hypothesis that voluntary exercise would ameliorate any deficits observed. Sprague-Dawley females were administered one of three diets throughout gestation: (i) ethanol (E), a liquid diet containing 36.5% ethanol-derived calories; (ii) pair-fed (PF), a liquid control diet, with maltose-dextrin isocalorically substituted for ethanol, in the amount consumed by an E partner (g/kg body wt/day of gestation); and (iii) ad-libitum-fed control (C), normal laboratory chow and water, ad libitum. The offspring were housed individually at postnatal day (PND) 35, and at PND 50 were randomly assigned to cages either with or without an exercise wheel. BrdU (200 mg/kg, I.P.) was injected on PND 57, and animals terminated either 24 h (proliferation) or 4 weeks (neurogenesis) later. Our results demonstrate that prenatal ethanol exposure significantly decreases both cell proliferation and neurogenesis in the adult dentate gyrus. Animals in the PF condition also showed reduced neurogenesis. In contrast, all animals that engaged in voluntary exercise showed a significant increase in cell proliferation and neurogenesis. These results indicate that prenatal ethanol exposure can suppress both cell proliferation and neurogenesis, and that these effects may be, at least in part, nutritionally mediated. Importantly, voluntary exercise appears to have beneficial effects for these long-lasting deficits in hippocampal volume and cell number that have been observed in animals exposed to ethanol in utero., ((c) 2006 Wiley-Liss, Inc.)
- Published
- 2006
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