Environmental enrichment (EE) and voluntary exercise (VEx) have consistently been shown to increase adult hippocampal neurogenesis and improve spatial learning ability. Although it appears that these two manipulations are equivalent in this regard, evidence exists that EE and VEx affect different phases of the neurogenic process in distinct ways. We review the data suggesting that EE increases the likelihood of survival of new cells, whereas VEx increases the level of proliferation of progenitor cells. We then outline the factors that may mediate these relationships. Finally, we provide a model showing that VEx leads to the convergence of key somatic and cerebral factors in the dentate gyrus (DG) to induce cell proliferation. Although insufficient evidence exists to provide a similar model for EE, we suggest that EE-induced cell survival in the DG involves cortical restructuring as a means of promoting survival. We conclude that EE and VEx lead to an increase in overall hippocampal neurogenesis via dissociable pathways, and should therefore, be considered distinct interventions with regard to hippocampal plasticity and associated behaviors.
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.
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