Ethanol neurotoxicity in culture: Selective loss of cholinergic neurons

Kentroti, Susan; Vernadakis, Antonia

doi:10.1002/(sici)1097-4547(19960615)44:6<577::aid-jnr8>3.0.co;2-8

Cited by 13 publications

(4 citation statements)

References 28 publications

(30 reference statements)

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“…This is consistent with in ovo and in vitro studies of neurons with specific neurotransmitter phenotypes [Kentroti and Vernadakis, 1992; 1995; 1996] and in vivo studies of cortical local circuit neurons expressing different calcium-binding proteins [Granato, 2006; Cuzon et al, 2008]. The latter studies are interesting in that they show that chronic prenatal exposure to ethanol causes changes that diametrically differ from changes induced by early postnatal exposure.…”

Section: Discussionsupporting

confidence: 83%

“…Among the cells in the embryonic telencephalic wall are proliferating pluripotential cells, i.e., neural stem cells [Kentroti and Vernadakis, 1992, 1995]. Some evidence supports the possibility that ethanol causes a selective elimination of cells with a particular lineage (i.e., after lineages are determined, yet discrimination is undetectable) [Kentroti and Vernadakis, 1996]. Based on other evidence, it can be argued that ethanol causes cells to switch their fates [Brodie and Vernadakis, 1992; Kentroti and Vernadakis, 1992].…”

Section: Introductionmentioning

confidence: 99%

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

Miller¹,

2009

Dev Neurosci

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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.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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

Miller¹,

2009

Dev Neurosci

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“…Specifically, experiments using ex vivo and in in vivo models have demonstrated that alcohol exposure during gestational periods affects NCAMs. Almost 30 years ago, it was reported that alcohol exposure (10 mg/50 microliters/day) to chick embryos at embryonic day 1–3 (E1-3) induced a significant increase of PSA-NCAM expression measured via Western blot in cerebral hemispheres between E8 and E10; while no significant change was observed in cerebellum from E10 to E20 ( Kentroti and Vernadakis, 1996 ). Moreover, in cortical cultures NCAMs were found to have altered neuronal growth patterns after alcohol exposure.…”

Section: Neural Cell Adhesion Molecule: Structure and Functionmentioning

confidence: 99%

“…To characterize the possible effects after alcohol exposure, cells were double-stained for NCAM and neurofilament, and the data collected showed changes in growth patterns of developing neurons and an intense NCAM staining. Interestingly, the altered NCAM expression in cerebral hemispheres corresponds temporally with the shift in neuronal phenotype from cholinergic to catecholaminergic and GABAergic ( Kentroti et al, 1995 ; Kentroti and Vernadakis, 1996 ). Taken together, these data suggest the effects of alcohol on neuronal growth patterns and on NCAM expression might influence the establishment of neurotransmitter phenotype.…”

Section: Neural Cell Adhesion Molecule: Structure and Functionmentioning

confidence: 99%

Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development

Licheri

Brigman

2021

Front. Mol. Neurosci.

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Alcohol exposure during pregnancy disrupts the development of the brain and produces long lasting behavioral and cognitive impairments collectively known as Fetal Alcohol Spectrum Disorders (FASDs). FASDs are characterized by alterations in learning, working memory, social behavior and executive function. A large body of literature using preclinical prenatal alcohol exposure models reports alcohol-induced changes in architecture and activity in specific brain regions affecting cognition. While multiple putative mechanisms of alcohol’s long-lasting effects on morphology and behavior have been investigated, an area that has received less attention is the effect of alcohol on cell adhesion molecules (CAMs). The embryo/fetal development represents a crucial period for Central Nervous System (CNS) development during which the cell-cell interaction plays an important role. CAMs play a critical role in neuronal migration and differentiation, synaptic organization and function which may be disrupted by alcohol. In this review, we summarize the physiological structure and role of CAMs involved in brain development, review the current literature on prenatal alcohol exposure effects on CAM function in different experimental models and pinpoint areas needed for future study to better understand how CAMs may mediate the morphological, sensory and behavioral outcomes in FASDs.

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Neuronal Plasticity in Development: Lessons from Ethanol Neurotoxicity during Embryogenesis

Kentroti

1997

Advances in Experimental Medicine and Biology

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Ethanol neurotoxicity in culture: Selective loss of cholinergic neurons

Cited by 13 publications

References 28 publications

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

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

Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development

Neuronal Plasticity in Development: Lessons from Ethanol Neurotoxicity during Embryogenesis

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