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Related Experiment Video

Updated: May 8, 2026

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
19:57

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

Long-lasting neural circuit dysfunction following developmental ethanol exposure.

Benjamin Sadrian1, Donald A Wilson, Mariko Saito

  • 1Department of Child and Adolescent Psychiatry, New York University Langone School of Medicine, One Park Avenue, Eighth Floor, New York, NY 10128, USA ; Nathan Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA.

Brain Sciences
|September 13, 2013
PubMed
Summary

Fetal Alcohol Spectrum Disorder (FASD) stems from prenatal alcohol exposure, causing lasting neurobehavioral and cognitive deficits. Research suggests ethanol disrupts neural development, leading to an excitation/inhibition imbalance and neurobehavioral pathology.

Keywords:
FASDalcoholbrain developmentexcitation/inhibition balanceneural circuitneurodegeneration

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Last Updated: May 8, 2026

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Quantification of Ethanol Levels in Zebrafish Embryos Using Head Space Gas Chromatography
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Published on: February 11, 2020

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Toxicology

Background:

  • Fetal Alcohol Spectrum Disorder (FASD) is a leading cause of mental deficits, resulting from prenatal alcohol exposure.
  • Understanding the neuropathology of FASD is crucial for developing effective human therapies.
  • Recent research models ethanol's impact on early neural circuit development.

Purpose of the Study:

  • To review current knowledge of FASD neuropathology.
  • To discuss the role of synaptic excitation and inhibition balance in FASD.
  • To explore how ethanol-induced neurodegeneration contributes to neurobehavioral deficits.

Main Methods:

  • Review of existing research findings on FASD neuropathology.
  • Analysis of animal models detailing neurophysiological effects of developmental ethanol exposure.
  • Discussion of synaptic plasticity and neural network function.

Main Results:

  • Ethanol exposure during development can cause long-lasting neurodegeneration.
  • This neurodegeneration impacts early neural circuit development and integration.
  • An imbalance between synaptic excitation and inhibition is implicated in FASD.

Conclusions:

  • Early ethanol-induced neurodegeneration perturbs neural development and function.
  • This disruption leads to an excitation/inhibition imbalance in the brain.
  • The resulting network signaling alterations underlie the neurobehavioral pathology observed in FASD.