Chronic prenatal ethanol exposure increases apoptosis in the hippocampus of the term fetal guinea pig

Green, C.R.; Kobus, Susan M.; Ji, Yin; Bennett, Brian M.; Reynolds, James N.; Brien, James F.

doi:10.1016/j.ntt.2005.07.006

Cited by 26 publications

(11 citation statements)

References 41 publications

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“…36 To confirm that activation of AMPK can protect against ethanol-induced apoptosis, we also examined the effect of co-administration of metformin and ethanol. As shown in Figure 7, metformin reduced the toxic effect of ethanol as measured by annexin V–PI staining.…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

et al. 2014

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Fetal alcohol syndrome is a neurological and developmental disorder caused by exposure of developing brain to ethanol. Administration of osmotin to rat pups reduced ethanol-induced apoptosis in cortical and hippocampal neurons. Osmotin, a plant protein, mitigated the ethanol-induced increases in cytochrome c, cleaved caspase-3, and PARP-1. Osmotin and ethanol reduced ethanol neurotoxicity both in vivo and in vitro by reducing the protein levels of cleaved caspase-3, intracellular [Ca2+]cyt, and mitochondrial transmembrane potential collapse, and also upregulated antiapoptotic Bcl-2 protein. Osmotin is a homolog of adiponectin, and it controls energy metabolism via phosphorylation. Adiponectin can protect hippocampal neurons against ethanol-induced apoptosis. Abrogation of signaling via receptors AdipoR1 or AdipoR2, by transfection with siRNAs, reduced the ability of osmotin and adiponectin to protect neurons against ethanol-induced neurodegeneration. Metformin, an activator of AMPK (adenosine monophosphate-activated protein kinase), increased whereas Compound C, an inhibitor of AMPK pathway, reduced the ability of osmotin and adiponectin to protect against ethanol-induced apoptosis. Osmotin exerted its neuroprotection via Bcl-2 family proteins and activation of AMPK signaling pathway. Modulation of AMPK pathways by osmotin, adiponectin, and metformin hold promise as a preventive therapy for fetal alcohol syndrome.

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Section: Resultsmentioning

confidence: 99%

Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

et al. 2014

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“…The use of varying alcohol treatment regimens in animal models has been critical for elucidating the teratogenic effects of alcohol. Regimens may involve acute maternal administration (i.e., 1 or 2 doses) during critical periods of fetal development (Sulik et al 1981; Godin et al 2010; Idrus and Napper 2012), trimester-equivalent fetal and (or) neonatal alcohol exposure (Bake et al 2012; Hamilton et al 2012; Wagner et al 2013; Jablonski and Stanton 2014), intermittent binge-like exposure (Ramadoss et al 2008; Sawant et al 2013), or chronic exposure throughout gestation through gavage, inhalation, or liquid diets (Lee et al 2000; Green et al 2005; Iqbal et al 2005, 2006; Hellemans et al 2010; Probyn et al 2013; Uban et al 2013). …”

Section: Risk Factors For Alcohol Teratogenicity and Fasdmentioning

confidence: 99%

Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE

Petrelli

Weinberg

Hicks

2018

Biochem. Cell Biol.

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The potential impact of prenatal alcohol exposure (PAE) varies considerably among exposed individuals, with some displaying serious alcohol-related effects and many others showing few or no overt signs of fetal alcohol spectrum disorder (FASD). In animal models, variables such as nutrition, genetic background, health, other drugs, and stress, as well as dosage, duration, and gestational timing of exposure to alcohol can all be controlled in a way that is not possible in a clinical situation. In this review we examine mouse models of PAE and focus on those with demonstrated craniofacial malformations, abnormal brain development, or behavioral phenotypes that may be considered FASD-like outcomes. Analysis of these data should provide a valuable tool for researchers wishing to choose the PAE model best suited to their research questions or to investigate established PAE models for FASD comorbidities. It should also allow recognition of patterns linking gestational timing, dosage, and duration of PAE, such as recognizing that binge alcohol exposure(s) during early gestation can lead to severe FASD outcomes. Identified patterns could be particularly insightful and lead to a better understanding of the molecular mechanisms underlying FASD.

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“…Results from these studies have indicated that PNEE can cause structural (101, 196–198), functional (103), and cognitive deficits (102, 103, 195) that mimic the human condition. These deficits were observed in neonate (101, 102, 196, 198), adolescent (197, 198), and adult (102, 103, 197, 198) animals. There has been only one study where ethanol administration has been restricted to the third trimester equivalent (classified as GD 43–62) (99) and surprisingly, hippocampal synaptic plasticity and spatial learning were not significantly affected in adult animals even with BACs of 245 mg/dl (99).…”

Section: Factors To Consider When Modeling Fasdmentioning

confidence: 99%

A Comparison of the Different Animal Models of Fetal Alcohol Spectrum Disorders and Their Use in Studying Complex Behaviors

2014

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Prenatal ethanol exposure (PNEE) has been linked to widespread impairments in brain structure and function. There are a number of animal models that are used to study the structural and functional deficits caused by PNEE, including, but not limited to invertebrates, fish, rodents, and non-human primates. Animal models enable a researcher to control important variables such as the route of ethanol administration, as well as the timing, frequency and amount of ethanol exposure. Each animal model and system of exposure has its place, depending on the research question being undertaken. In this review, we will examine the different routes of ethanol administration and the various animal models of fetal alcohol spectrum disorders (FASD) that are commonly used in research, emphasizing their strengths and limitations. We will also present an up-to-date summary on the effects of prenatal/neonatal ethanol exposure on behavior across the lifespan, focusing on learning and memory, olfaction, social, executive, and motor functions. Special emphasis will be placed where the various animal models best represent deficits observed in the human condition and offer a viable test bed to examine potential therapeutics for human beings with FASD.

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Chronic prenatal ethanol exposure increases apoptosis in the hippocampus of the term fetal guinea pig

Cited by 26 publications

References 41 publications

Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE

A Comparison of the Different Animal Models of Fetal Alcohol Spectrum Disorders and Their Use in Studying Complex Behaviors

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