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Research ArticleNew Research, Disorders of the Nervous System

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry

Emma L. Louth, Warren Bignell, Christine L. Taylor and Craig D.C. Bailey
eNeuro 27 October 2016, 3 (5) ENEURO.0267-16.2016; DOI: https://doi.org/10.1523/ENEURO.0267-16.2016
Emma L. Louth
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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Warren Bignell
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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Christine L. Taylor
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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Craig D.C. Bailey
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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Abstract

Chronic prenatal exposure to ethanol can lead to a spectrum of teratogenic outcomes that are classified in humans as fetal alcohol spectrum disorders (FASD). One of the most prevalent and persistent neurocognitive components of FASD is attention deficits, and it is now thought that these attention deficits differ from traditional attention deficit hyperactivity disorder (ADHD) in their quality and response to medication. However, the neuronal mechanisms underlying attention deficits in FASD are not well understood. We show here that after developmental binge-pattern ethanol exposure, adult mice exhibit impaired performance on the five-choice serial reaction time test for visual attention, with lower accuracy during initial training and a higher rate of omissions under challenging conditions of high attention demand. Whole-cell electrophysiology experiments in these same mice find dysregulated pyramidal neurons in layer VI of the medial prefrontal cortex, which are critical for normal attention performance. Layer VI neurons show decreased intrinsic excitability and increased responses to stimulation of both nicotinic acetylcholine receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors. Moreover, although nicotinic acetylcholine responses correlate with performance on the five-choice task in control mice, these relationships are completely disrupted in mice exposed to ethanol during development. These findings demonstrate a novel outcome of developmental binge-pattern ethanol exposure and suggest that persistent alterations to the function of prefrontal layer VI neurons play an important mechanistic role in attention deficits associated with FASD.

  • attention
  • developmental ethanol exposure
  • electrophysiology
  • fetal alcohol spectrum disorders
  • nicotinic receptors
  • prefrontal cortex

Footnotes

  • The authors declare no competing financial interests.

  • This work was supported by grants to C.D.C.B. from the Banting Research Foundation, the Natural Sciences and Engineering Research Council of Canada (NSERC Discovery Grant number 436190), and the Canada Foundation for Innovation (CFI Project number 30381). E.L.L. was supported by an Ontario Graduate Scholarship and an OVC Scholarship from the Ontario Veterinary College at the University of Guelph.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry
Emma L. Louth, Warren Bignell, Christine L. Taylor, Craig D.C. Bailey
eNeuro 27 October 2016, 3 (5) ENEURO.0267-16.2016; DOI: 10.1523/ENEURO.0267-16.2016

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Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry
Emma L. Louth, Warren Bignell, Christine L. Taylor, Craig D.C. Bailey
eNeuro 27 October 2016, 3 (5) ENEURO.0267-16.2016; DOI: 10.1523/ENEURO.0267-16.2016
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Keywords

  • attention
  • Developmental Ethanol Exposure
  • electrophysiology
  • Fetal Alcohol Spectrum Disorders
  • nicotinic receptors
  • prefrontal cortex

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