54: Prevention of the alcohol-induced changes in brain-derived neurotrophic factor expression using neuroprotective peptides in a model of fetal alcohol syndrome

Abstract

ObjectiveFetal alcohol syndrome (FAS) is the most common non genetic cause of mental retardation; prenatal alcohol exposure affects the development of the nervous system. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that is essential in normal neuronal development and survival as well as synaptic plasticity, an important factor in learning and memory. Previously, we have shown that prenatal treatment with neuroprotective peptides, NAP+SAL, prevented alcohol induced fetal anomalies and learning deficits. Our objective was to evaluate if NAP+SAL′s neuroprotective effects are mediated by preventing alcohol-induced changes in BDNF expression during embryonic development.Study DesignA well-characterized FAS model was used (Webster, 1980). Timed, pregnant C57BL6/J mice were treated on gestational day 8 (E8) with alcohol (0.03 mL/g), placebo or alcohol+peptides (20g, 30 min before alcohol). Embryos were harvested at 6h(E8), 24h(E9) and day 10(E18). Each sample included at least 3 embryos, representing at least 3 litters per time point. Calibrator-normalized relative real-time PCR was performed to quantify BDNF with HPRT1 standardization. Statistics included ANOVA and Fisher PLSD.ResultsConclusionNAP+SAL prevented alcohol-induced changes in BDNF expression 24h and 10 days after alcohol exposure. This may explain, at least in part, the peptides prevention of neurodevelopmental anomalies and learning deficits in fetal alcohol syndrome. ObjectiveFetal alcohol syndrome (FAS) is the most common non genetic cause of mental retardation; prenatal alcohol exposure affects the development of the nervous system. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that is essential in normal neuronal development and survival as well as synaptic plasticity, an important factor in learning and memory. Previously, we have shown that prenatal treatment with neuroprotective peptides, NAP+SAL, prevented alcohol induced fetal anomalies and learning deficits. Our objective was to evaluate if NAP+SAL′s neuroprotective effects are mediated by preventing alcohol-induced changes in BDNF expression during embryonic development. Fetal alcohol syndrome (FAS) is the most common non genetic cause of mental retardation; prenatal alcohol exposure affects the development of the nervous system. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that is essential in normal neuronal development and survival as well as synaptic plasticity, an important factor in learning and memory. Previously, we have shown that prenatal treatment with neuroprotective peptides, NAP+SAL, prevented alcohol induced fetal anomalies and learning deficits. Our objective was to evaluate if NAP+SAL′s neuroprotective effects are mediated by preventing alcohol-induced changes in BDNF expression during embryonic development. Study DesignA well-characterized FAS model was used (Webster, 1980). Timed, pregnant C57BL6/J mice were treated on gestational day 8 (E8) with alcohol (0.03 mL/g), placebo or alcohol+peptides (20g, 30 min before alcohol). Embryos were harvested at 6h(E8), 24h(E9) and day 10(E18). Each sample included at least 3 embryos, representing at least 3 litters per time point. Calibrator-normalized relative real-time PCR was performed to quantify BDNF with HPRT1 standardization. Statistics included ANOVA and Fisher PLSD. A well-characterized FAS model was used (Webster, 1980). Timed, pregnant C57BL6/J mice were treated on gestational day 8 (E8) with alcohol (0.03 mL/g), placebo or alcohol+peptides (20g, 30 min before alcohol). Embryos were harvested at 6h(E8), 24h(E9) and day 10(E18). Each sample included at least 3 embryos, representing at least 3 litters per time point. Calibrator-normalized relative real-time PCR was performed to quantify BDNF with HPRT1 standardization. Statistics included ANOVA and Fisher PLSD. Results ConclusionNAP+SAL prevented alcohol-induced changes in BDNF expression 24h and 10 days after alcohol exposure. This may explain, at least in part, the peptides prevention of neurodevelopmental anomalies and learning deficits in fetal alcohol syndrome. NAP+SAL prevented alcohol-induced changes in BDNF expression 24h and 10 days after alcohol exposure. This may explain, at least in part, the peptides prevention of neurodevelopmental anomalies and learning deficits in fetal alcohol syndrome.