Lability of Neuronal Lineage Decisions Is Revealed by Acute Exposures to Ethanol

Abstract

On August 6, 2010, the Editor-in-Chief of Developmental Neuroscience, Steven W. Levison, was contacted by the legal counsel for SUNY Upstate Medical University and informed that an investigative committee at SUNY Upstate had determined that Dr. Michael Miller was guilty of multiple counts of research misconduct, and they requested that Developmental Neuroscience retract the 2009 article authored by Drs. Miller and Huaiyu Hu. The committee did not find Dr. Hu at fault for any scientific misconduct. After independently reviewing the reports of the investigative committee and the rebuttals provided by Dr. Miller, the Editor-in-Chief and the publisher concurred that there were errors in reporting sample sizes and in mathematical calculations. However, at that time it was our view that an erratum was more appropriate than a retraction of the article. Despite the flaws in the analyses of the data, it was our determination that those flaws could be corrected in a published erratum to produce a final product that would be more useful to the scientific community than a complete retraction of the work. On December 10, 2010, we requested that Dr. Miller provide a corrected figure with an explanation of the mistakes that had been previously published. However, that erratum was never published as we were provided with additional information and testimonies that convinced us that the collected data may also be unreliable. Accordingly, on October 18, 2011, we requested that a letter of retraction be provided that was co-authored and co-signed by both authors. It was our view that for an action as severe as an article retraction, both authors needed to sign the retraction letter. However, Drs. Miller and Hu were unable to agree upon a letter that could be jointly signed. Therefore, at the request of the President of SUNY Upstate, with this statement we formally retract the article by Drs. Miller and Hu, Developmental Neuroscience 2009;31:50–57. We have sent correspondence to both authors, to the President of SUNY Upstate and to Dr. Steven Goodman, Vice President for Research at SUNY Upstate, to inform them in advance that this action is being taken by the journal.

Combined transcriptome analysis of fetal human and mouse cerebral cortex exposed to alcohol

“…The disruption of molecular identity in lower layers is unlikely due to altered neuronal production, because most lower layer neurons are produced before the embryos were exposed to ethanol at E14. Differential vulnerability of various neuronal subtypes to alcohol stress might be another mechanism (12,53).…”

Enforced Pax6 Expression Rescues Alcohol‐Induced Defects of Neuronal Differentiation in Cultures of Human Cortical Progenitor Cells

“…In monkey, the percentage of glutaminergic and GABAergic neurons in the somatosensory cortex did not change after in utero exposure to EtOH, but the overall number of cortical neurons was significantly reduced, suggesting that the primary detrimental effect of EtOH is on neuronal precursor (Miller and Spear, ). Studies in rodents with a short interval of EtOH exposure at various embryonic days showed that the effect was less pronounced on the generation of neurons and their survival, but cell lineage could be switched during terminal division and even some time after that (Miller and Hu, ). In another report, EtOH was found to negatively affect proliferation of interneuron progenitors in medial ganglionic eminence, whereas differentiation into GABAergic cells and their tangential migration was increased, resulting in more GABAergic cells in embryonic cortex (Cuzon et al., ).…”

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

“…Several studies have identified effects of low amounts of alcohol exposure on the development of serotonergic neurons (Sari and Zhou, 2004;Zhou et al, 2003;Zhou et al, 2005), and suggested that these types of defects in the ontogeny of a specific neurotransmitter system may underlie the more 'subtle' deficits observed in human children diagnose with Alcohol Related Neurodevelopmental Disorder, rather than fullblown FAS (Zhou et al, 2003). Ethanol exposure disrupts the proliferation of glia and neuronal precursors in the developing central nervous system (Luo and Miller, 1998;Miller, 2007;Miller and Hu, 2009;Powrozek and Miller, 2009) and can dramatically alter behavior (Hellemans et al, 2010;Valenzuela et al, 2012). Transcriptional analyses of gene products regulated by fetal ethanol exposure in both mouse and human cells also highlight genes related to neural development, such as cell proliferation, neuronal migration, and differentiation (Hashimoto-Torii et al, 2011;Hicks et al, 2010).…”