In vitro Neurogenesis from Neural Progenitor Cells Isolated from the Hippocampus Region of the Brain of Adult Rats Exposed to Ethanol during Early Development through Their Alcohol-Drinking Mothers

Abstract

Neuronal maturation was significantly delayed in ethanol-exposed rats. AC(o) NPCs, up to day 7 of culture, exhibited high beta-catenin-probe binding, an increase in Ca(2+) when exposed to gamma-amino butyric acid (GABA) and lack of response to glutamate (Glu) exposure. beta-Catenin-probe binding and the stimulatory effects of GABA declined thereafter. AC(o) NPCs, at culture day 29, exhibited high beta-catenin-probe binding, lack of response to GABA and elevated Glu-induced increase in Ca(2+i). Cultures of AE(o) NPCs showed an amplified stimulatory effects of GABA, attenuated stimulatory effects of Glu and attenuated the delayed (culture day 29) increase in the expression of Wnt proteins and beta-catenin-probe binding. This suggests a significant alteration in neurogenesis and synapse formation in adult rats exposed to ethanol at early development through their alcohol-drinking mothers.

Calcium-mediated repression of β-catenin and its transcriptional signaling mediates neural crest cell death in an avian model of fetal alcohol syndrome

“…This may be secondary due to the commensurate loss of BMP activity, although acute ethanol can also rapidly deplete nuclear β-catenin from osteoblasts (Chen et al 2010), a finding consistent with our own studies with neural crest progenitors. For neurons the findings are contradictory, with chronic ethanol exposure reducing the total β-catenin content of cultured hippocampal neurons (Singh et al 2009) but elevating β-catenin in the frontal cortex of chronic alcoholics (Al-Housseini et al 2008). These neuronal studies did not distinguish between the cytoskeletal and nuclear pools and thus the functional consequences of those changes are uncertain.…”

Regulation of Adult Neurogenesis and Plasticity by (Early) Stress, Glucocorticoids, and Inflammation

“…Finally, it is important to mention that levels of neurogenesis are permanently affected also by other ELS not necessarily related to the mother-infant interaction alone. For example, ELS inflammation (Jakubs et al 2008;Musaelyan et al 2014), radiation therapy (Fukuda et al 2005;Naylor et al 2008;Hoffman and Yock 2009), anesthesia (Zhu et al 2010), stroke (Spadafora et al 2010), infection (Bland et al 2010), and ethanol exposure (Singh et al 2009) induce long-lasting effects on neurogenesis associated with late-onset cognitive impairment. Thus, the studies described have shown that EL experiences during both pre-and postnatal development can bidirectionally alter hippocampal neuronal plasticity and synaptic integrity.…”

Screening, Diagnosing and Prevention of Fetal Alcohol Syndrome: Is This Syndrome Treatable

“…They observed reduced neurite branching and increased primary neurite length in ethanol-pretreated differentiating neurons in the proliferative phase [Camarillo et al, 2008]. Most recently, Singh et al [2009] described several molecular changes in neurogenesis found in embryonic rodents exposed to alcohol. The focus of the study was on Wnt-␤ -catenin and its role in ethanol-induced changes in neurogenesis.…”