Environmental Enrichment Alters Neurotrophin Levels After Fetal Alcohol Exposure in Rats

Department of Neurological Surgery, University of California, Davis, California 95616, USA.
Alcoholism Clinical and Experimental Research (Impact Factor: 3.21). 10/2008; 32(10):1741-51. DOI: 10.1111/j.1530-0277.2008.00759.x
Source: PubMed


Prenatal alcohol exposure causes abnormal brain development, leading to behavioral deficits, some of which can be ameliorated by environmental enrichment. As both environmental enrichment and prenatal alcohol exposure can individually alter neurotrophin expression, we studied the interaction of prenatal alcohol and postweaning environmental enrichment on brain neurotrophin levels in rats.
Pregnant rats received alcohol by gavage, 0, 4, or 6 g/kg/d (Zero, Low, or High groups), or no treatment (Naïve group), on gestational days 8 to 20. After weaning on postnatal day 21, offspring were housed for 6 weeks in Isolated, Social, or Enriched conditions. Levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) were then measured in frontal cortex, occipital cortex, hippocampus, and cerebellar vermis.
Prenatal alcohol exposure increased NGF levels in frontal cortex (High-dose group) and cerebellar vermis (High- and Low-dose groups); increased BDNF in frontal cortex, occipital cortex and hippocampus (Low-dose groups), and increased NT-3 in hippocampus and cerebellar vermis (High-dose). Environmental enrichment resulted in lower NGF, BDNF, and NT-3 levels in occipital cortex and lower NGF in frontal cortex. The only significant interaction between prenatal alcohol treatment and environment was in cerebellar vermis where NT-3 levels were higher for enriched animals after prenatal alcohol exposure, but not for animals housed under Isolated or Social conditions.
Both prenatal alcohol exposure and postweaning housing conditions alter brain neurotrophin levels, but the effects appear to be largely independent. Although environmental enrichment can improve functional outcomes, these results do not provide strong support for the hypothesis that rearing in a complex environment ameliorates prenatal alcohol effects on brain neurotrophin levels in rats.

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    • "Prenatal ethanol exposure associated with reduced BDNF mRNA level in hippocampal formation has previously been reported (Caldwell et al., 2008). However , the reduction of BDNF protein level in the hippocampus appeared to be limited to male rat (Parks et al., 2008). In the striatum, previous study showed that prenatal alcohol exposure at the dose of 1 g/kg/day did not significantly affect BDNF protein levels but at the dose of 3 g/kg/day markedly reduced levels of BDNF protein and mRNA in the hippocampus of offspring (Feng et al., 2005). "
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    ABSTRACT: Prenatal exposure to alcohol can result in fetal alcohol syndrome (FAS), characterized by significant changes in the physiology, structural plasticity of hippocampal function, including long-term deficits in learning and memory. Environmental enrichment has long been known to improve motor and cognitive function levels, causes several neurochemical and morphological alterations in the brain. Therefore, the effects of environmental enrichment on the neurobehavioral and neurotrophic changes in mice exposed prenatally to alcohol were investigated in this study. The pregnant dams were given 25 % ethanol (w/v) or isocaloric sucrose by liquid diet from gestation day 7 to 20. After we aning on postnatal day 28, offspring were exposed to standard cage (CC, CFAS) or enriched living conditions (CE, EFAS) for 8 weeks. Neurobehavioral studies both on hippocamus-dendent spatial learning and place and cue learning strategy, a striatum-dependent test, were measured by the Morris water maze task. Moreover, the reverse-transcriptase polymerase chain reaction (RT-PCR) technique was also used in order to study the expression of brain-derived neurotrophic factor (BDNF) level in both the hippocampus and striatum of mice. Neurobehavioral studies show that animals exposed prenatally to alcohol were impaired as shown in both hippocampal-dependent spatial/place and striatal-dependent response/cue learning tests. Moreover, the levels of BDNF expression both in the hippocampus and striatum of mice were also decreased. Interestingly, environmental enrichment can ameliorate the effects of prenatal alcohol exposure both on the neurobehavioral and neurotrophic levels. These observations indicated that enriched environment attenuated memory impairment of prenatal alcohol exposure both in hippocampal and striatal circuitry.
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    • "Exposure to enriched housing condition reduced the amount of spontaneous steethanol-exposed animals following environmental enrichment has not been documented (Berman et al. 1996; Parks et al. 2008; Wainwright et al. 1993). Lastly, Down syndrome is a common genetic cause of mental retardation, and is often accompanied by behavioral disorders and attention deficits (Visootsak and Sherman 2007). "
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    ABSTRACT: The field of behavioral neuroscience has been successful in using an animal model of enriched environments for over five decades to measure the rehabilitative and preventative effects of sensory, cognitive and motor stimulation in animal models. Several key principles of enriched environments match those used in sensory integration therapy, a treatment used for children with neurodevelopmental disorders. This paper reviews the paradigm of environmental enrichment, compares animal models of enriched environments to principles of sensory integration treatment, and discusses applications for the rehabilitation of neurodevelopmental disorders. Based on this review, the essential features in the enriched environment paradigm which should be included in sensory integration treatment are multiple sensory experiences, novelty in the environment, and active engagement in challenging cognitive, sensory, and motor tasks. Use of sensory integration treatment may be most applicable for children with anxiety, hypersensitivity, repetitive behaviors or heightened levels of stress. Additionally, individuals with deficits in social behavior, social participation, or impairments in learning and memory may show gains with this type of treatment.
    Preview · Article · Sep 2010 · Journal of Neurodevelopmental Disorders
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    ABSTRACT: The authors study a rapid coherent acquisition scheme, using a truncated sequential-probability-ratio test (TSPRT), for direct-sequence-spread spectrum (DS/SS) systems. Since the partial correlation of pseudonoise (PN) sequences is difficult to characterize, the worst-case partial correlation is considered. Linearized bounds of the partial correlation are used for designing the TSPRT so that the resulting test can achieve the prescribed acquisition condition. The design parameters of the TSPRT are chosen so that the average sample size (ASN) is minimized while keeping the maximum ASN smaller than that of the fixed dwell scheme with similar false alarm and miss probabilities. Some simulation results are obtained, and they agree well with analytic results
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