Effects of prenatal ethanol exposure on rat brain radial glia and neuroblast migration

Aronne, María Paula; Guadagnoli, Tamara; Fontanet, Paula; Evrard, Sergio Gustavo; Brusco, Alicia

doi:10.1016/j.expneurol.2011.03.002

Cited by 49 publications

(41 citation statements)

References 40 publications

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“…However, GAD1 suppression in limited periods of development or in restricted cell types has multiple consequences. Disrupting GABA signaling during early development alters cellular migration and cortical architecture in cell type-dependent ways (Aronne et al, 2011;Cuzon et al, 2008;Haas et al, 2013;Manent et al, 2007;Thompson et al, 2009;Wu et al, 2012). PV þ interneurons are selectively disrupted by exogenous GABA potentiation (Haas et al, 2013;Levav-Rabkin et al, 2010).…”

Section: Gene Effects Converge Onto Gaba System Developmentmentioning

confidence: 99%

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Schmidt

Mirnics

2014

Neuropsychopharmacol

196

130

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The origins of schizophrenia have eluded clinicians and researchers since Kraepelin and Bleuler began documenting their findings. However, large clinical research efforts in recent decades have identified numerous genetic and environmental risk factors for schizophrenia. The combined data strongly support the neurodevelopmental hypothesis of schizophrenia and underscore the importance of the common converging effects of diverse insults. In this review, we discuss the evidence that genetic and environmental risk factors that predispose to schizophrenia disrupt the development and normal functioning of the GABAergic system.

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Section: Gene Effects Converge Onto Gaba System Developmentmentioning

confidence: 99%

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Schmidt

Mirnics

2014

Neuropsychopharmacol

196

130

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“…Cortical volume, thickness, and surface area are reduced by ethanol exposure throughout gestation in rodents (Leigland et al, 2013). Proper neuron migration into the cerebral cortex is also disrupted by ethanol (Gressens, Lammens, Picard, & Evrard, 1992; Miller, 1993) apparently through inhibition of radial glia development and ethanol-induced changes in the expression of molecules central to migration (Aronne, Guadagnoli, Fontanet, Evrard, & Brusco, 2011; Miller & Robertson, 1993). Rodent models of fetal ethanol exposure further demonstrate neuroanatomical, synaptic, and electrophysiological defects in neocortical circuitry that correspond to deficits in behavior (El Shawa, Abbott, & Huffman, 2013; Inomata, Nasu, & Tanaka, 1987; Slawecki, Thomas, Riley, & Ehlers, 2004; Whitcher & Klintsova, 2008; Wilson et al, 2011).…”

Section: Fasd Neuropathology In Animal Modelsmentioning

confidence: 99%

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

Drew

Kane

2014

International Review of Neurobiology

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The behavioral consequences of fetal alcohol spectrum disorders (FASD) are serious and persist throughout life. The causative mechanisms underlying FASD are poorly understood. However, much has been learned about FASD from human structural and functional studies as well as from animal models, which have provided a greater understanding of the mechanisms underlying FASD. Using animal models of FASD, it has been recently discovered that ethanol induces neuroimmune activation in the developing brain. The resulting microglial activation, production of proinflammatory molecules, and alteration in expression of developmental genes are postulated to alter neuron survival and function and lead to long-term neuropathological and cognitive defects. It has also been discovered that microglial loss occurs, reducing microglia’s ability to protect neurons and contribute to neuronal development. This is important, because emerging evidence demonstrates that microglial depletion during brain development leads to long-term neuropathological and cognitive defects. Interestingly, the behavioral consequences of microglial depletion and neuroimmune activation in the fetal brain are particularly relevant to FASD. This chapter reviews the neuropathological and behavioral abnormalities of FASD and delineates correlates in animal models. This serves as a foundation to discuss the role of the neuroimmune system in normal brain development, the consequences of microglial depletion and neuroinflammation, the evidence of ethanol induction of neuroinflammatory processes in animal models of FASD, and the development of anti-inflammatory therapies as a new strategy for prevention or treatment of FASD. Together, this knowledge provides a framework for discussion and further investigation of the role of neuroimmune processes in FASD.

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“…There were no significant differences in body or brain weight between control mice (paired group) and those exposed to either 1 or 2 g∙kg −1 EtOH in a previous study 39 . We did not include a chow-fed group in the present study because no meaningful differences in corticogenesis between pair-fed and chow-fed groups have been observed in previous studies 3, 13 . Downing et al .…”

Section: Methodsmentioning

confidence: 99%

“…A vast array of adverse health effects—including mental, emotional, craniofacial, physiological, and immune disorders—have been documented, and research has revealed that EtOH induces apoptosis and inhibits neural stem cell proliferation in developing brain 1, 2 . Prenatal exposure to EtOH affects radial glial cell morphology, neuronal migration 3 , and induces cell death in layer V neurons 4 , particularly in the dorsal telencephalon. Recent research has also revealed that perinatal exposure to EtOH affects microglia during brain development 5 .…”

Section: Introductionmentioning

confidence: 99%

Mechanisms underlying neuro-inflammation and neurodevelopmental toxicity in the mouse neocortex following prenatal exposure to ethanol

Komada

Hara

Kawachi

et al. 2017

Sci Rep

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Fetal alcohol spectrum disorders (FASD) constitute a wide range of disorders that arise from prenatal exposure to ethanol (EtOH). However, detailed reports regarding the adverse effects of prenatal EtOH exposure on neocortical morphology and its underlying pathogenic mechanisms are limited. In the present study, we aimed to characterize the anatomical abnormalities of neocortical development and their correlation with microglial properties and neuro-inflammation in a mouse model of FASD. We evaluated the development and maturation of the neocortex in ICR mice prenatally exposed to 25% (w/v) EtOH using histological and molecular analyses. Reduced proliferation and excessive cell death were observed in the dorsal telencephalon. Abnormal neuronal distribution, layer formation, and dopaminergic neuronal projections were observed in the neocortex. Disruption of microglial differentiation (M1/M2 microglial ratio) and abnormal expression of pro-inflammatory and neurotrophic factors were induced, and these abnormalities were ameliorated by co-treatment with an anti-inflammatory drug (pioglitazone). FASD model mice displayed histological abnormalities, microglial abnormalities, and neuro-inflammation in both the embryonic and newborn stages. Thus, anti-inflammatory therapeutics may provide a novel preventive approach for the treatment of FASD.

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Effects of prenatal ethanol exposure on rat brain radial glia and neuroblast migration

Cited by 49 publications

References 40 publications

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

Mechanisms underlying neuro-inflammation and neurodevelopmental toxicity in the mouse neocortex following prenatal exposure to ethanol

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