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

Gabriel, Kara I.; Johnston, S. Y.; Weinberg, Joanne

doi:10.1002/dev.10023

Cited by 39 publications

(18 citation statements)

References 82 publications

(115 reference statements)

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“…In utero ethanol exposure or neonatal exposure during the brain growth spurt induces numerous cognitive and behavioral deficits. Of relevance to the current study are findings of impaired spatial learning and memory in the offspring (Blanchard et al, 1987;Kelly et al, 1988;Gianoulakis, 1990;Kim et al, 1997;Gabriel et al, 2002;Richardson et al, 2002;Savage et al, 2002;Iqbal et al, 2004;Christie et al, 2005), with animals exhibiting deficits similar to those observed following bilateral lesions of the hippocampus (Morris et al, 1982). In addition, long-term potentiation (LTP), a biological model for learning and memory processes, is also impaired in E animals (Sutherland et al, 1997;Richardson et al, 2002;Savage et al, 2002;Christie et al, 2005).…”

Section: Introductionmentioning

confidence: 65%

Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise

et al. 2006

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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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Section: Introductionmentioning

confidence: 65%

Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise

et al. 2006

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“…We did not use cross-fostering because dams in our model show no signs of malnutrition compared with normal (12,14). Furthermore, it has been suggested that fostering may confound the effects of prenatal EtOH exposure (28). Because of similar litter sizes between groups, we also refrained from culling pups as litter size manipulation has been shown to alter neuronal activity and the level of nutrition received during lactation (20).…”

Section: Methodsmentioning

confidence: 99%

Intrauterine ethanol exposure results in hypothalamic oxidative stress and neuroendocrine alterations in adult rat offspring

Dembele

Yao²,

Chen³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Dembele, Korami, Xing-Hai Yao, Li Chen and B. L. Grégoire Nyomba. Intrauterine ethanol exposure results in hypothalamic oxidative stress and neuroendocrine alterations in adult rat offspring. Am J Physiol Regul Integr Comp Physiol 291: R796 -R802, 2006. First published April 13, 2006 doi:10.1152/ajpregu.00633.2005 exposure is associated with low birth weight, followed by increased appetite, catch-up growth, insulin resistance, and impaired glucose tolerance in the rat offspring. Because EtOH can induce oxidative stress, which is a putative mechanism of insulin resistance, and because of the central role of the hypothalamus in the regulation of energy homeostasis and insulin action, we investigated whether prenatal EtOH exposure causes oxidative damage to the hypothalamus, which may alter its function. Female rats were given EtOH by gavage throughout pregnancy. At birth, their offspring were smaller than those of non-EtOH rats. Markers of oxidative stress and expression of neuropeptide Y and proopiomelanocortin (POMC) were determined in hypothalami of postnatal day 7 (PD7) and 3-mo-old (adult) rat offspring. In both PD7 and adult rats, prenatal EtOH exposure was associated with decreased levels of glutathione and increased expression of MnSOD. The concentrations of lipid peroxides and protein carbonyls were normal in PD7 EtOH-exposed offspring, but were increased in adult EtOH-exposed offspring. Both PD7 and adult EtOH-exposed offspring had normal neuropeptide Y and POMC mRNA levels, but the adult offspring had reduced POMC protein concentration. Thus only adult offspring preexposed to EtOH had increased hypothalamic tissue damage and decreased levels of POMC, which could impair melanocortin signaling. We conclude that prenatal EtOH exposure causes hypothalamic oxidative stress, which persists into adult life and alters melanocortin action during adulthood. These neuroendocrine alterations may explain weight gain and insulin resistance in rats exposed to EtOH early in life.

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“…Neonatal handling during the first 3 weeks, which involved daily separation from home cages and tactile stimulation, was effective in eliminating this learning deficit. Researchers have failed, however, to eliminate spatial memory deficits in alcoholexposed animals through neonatal handling (Gabriel et al 2002). Gabriel et al (2000) have also reported that neonatal handling was ineffective at ameliorating hypothalamicpituitary-adrenal hyperresponsiveness to stress and at normalizing hypothalamic corticotropin-releasing factor levels in alcohol-exposed animals.…”

Section: Neonatal Handlingmentioning

confidence: 96%

From Research to Practice: An Integrative Framework for the Development of Interventions for Children with Fetal Alcohol Spectrum Disorders

Kodituwakku

2011

Neuropsychol Rev

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Since fetal alcohol syndrome was first described over 35 years ago, considerable progress has been made in the delineation of the neurocognitive profile in children with prenatal alcohol exposure. Preclinical investigators have made impressive strides in elucidating the mechanisms of alcohol teratogenesis and in testing the effectiveness of pharmacological agents and dietary supplementation in the amelioration of alcohol-induced deficits. Despite these advances, only limited progress has been made in the development of evidence-based comprehensive interventions for functional impairment in alcohol-exposed children. Having performed a search in PubMed and PsycINFO using key words, interventions, treatment, fetal alcohol syndrome, prenatal alcohol exposure, and fetal alcohol spectrum disorders, we found only 12 papers on empirically-based interventions. Only two of these interventions had been replicated and none met the criteria of "well-established," as defined by Chambless and Hollon (Journal of Consulting and Clinical Psychology 66(1):7-18, 1998). There has been only limited cross-fertilization of ideas between preclinical and clinical research with regard to the development of interventions. Therefore, we propose a framework that allows integrating data from preclinical and clinical investigations to develop comprehensive intervention programs for children with fetal alcohol spectrum disorders. This framework underscores the importance of multi-level evaluations and interventions.

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

Cited by 39 publications

References 82 publications

Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise

Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise

Intrauterine ethanol exposure results in hypothalamic oxidative stress and neuroendocrine alterations in adult rat offspring

From Research to Practice: An Integrative Framework for the Development of Interventions for Children with Fetal Alcohol Spectrum Disorders

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