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.
"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). "
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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
Military Communications Conference, 1989. MILCOM '89. Conference Record. Bridging the Gap. Interoperability, Survivability, Security., 1989 IEEE; 11/1989
[Show abstract][Hide abstract] ABSTRACT: Neural crest cells (NCCs), a transient population that migrates from the developing neural tube, distributes through the embryo and differentiates into many derivatives, are clearly involved in the damage induced by prenatal exposure to ethanol. The aim of this work was to evaluate alterations of trophic parameters of in vivo (in ovo) and in vitro NCCs exposed to teratogenic ethanol doses, and their possible prevention by trophic factor treatment. Chick embryos of 24-30h of incubation were treated during 10h with 100mM ethanol, or 40 ng/ml Neurotrophin 3 (NT3), or 10 ng/ml Ciliary Neurotrophic Factor (CNTF), or ethanol plus NT3 or CNTF, or defined medium; then the topographic distribution of NCC apoptosis was assessed using a whole-mount acridine orange supravital method. Cultures of cephalic NCCs were exposed to the same ethanol or NT3, or CNTF treatments, or ethanol plus one of both trophic factors, or N2 medium. A viability assay was performed using the calcein-ethidium test, apoptosis was evaluated with the TUNEL test, and proliferative capacity after BrdU labeling. After direct exposure of embryos to 100mM ethanol for 10h, a high level of NCC apoptosis was coincident with the abnormal closure of the neural tube. These anomalies were prevented in embryos exposed to ethanol plus NT3 but not with CNTF. In NCC cultures, high cell mortality and a diminution of proliferative activity were observed after 3h of ethanol treatment. Incubation with ethanol plus NT3 (but not with CNTF) prevented NCC mortality as well as a fall in NCC proliferation. The consequences of direct exposure to ethanol expand data from our and other laboratories, supporting current opinion on the potential risk of alcohol ingestion (even at low doses and/or during a short time), in any period of pregnancy or lactation. Our in vivo/in vitro model encourages us to examine the pathogenic mechanism(s) of the ethanol-exposed embryo as well as the use of trophic factors for the treatment and/or prevention of anomalies induced by prenatal alcohol.
Neurotoxicology and Teratology 03/2011; 33(3):422-30. DOI:10.1016/j.ntt.2011.03.003 · 2.76 Impact Factor
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