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

Balapal S Basavarajappa1,2,3,4, Shivakumar Subbanna1

  • 1Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.

Cells
|February 11, 2023
PubMed
Summary

Synaptic plasticity alterations contribute to neurobehavioral issues in fetal alcohol spectrum disorder (FASD). Understanding these changes offers potential therapeutic targets for FASD-related cognitive and behavioral impairments.

Keywords:
alcoholcognitive behaviorgene expressionintellectual disabilitieslearning and memoryneurotransmitterpregnancyprotein expressionreceptorssynaptic structure

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Synaptic plasticity, the brain's ability to modify connections, is crucial for remodeling after brain damage.
  • Alcohol use disorders (AUDs) and prenatal alcohol exposure significantly impact central nervous system (CNS) development, leading to fetal alcohol spectrum disorder (FASD).
  • While synaptic plasticity is studied, its role in the neurobehavioral abnormalities of AUDs and FASD remains incompletely understood.

Purpose of the Study:

  • To review research on synaptic and molecular changes in FASD.
  • To elucidate the mechanisms of synaptic dysfunction in FASD.
  • To identify potential synaptic targets for treating FASD-related neurobehavioral abnormalities.

Main Methods:

  • Review of existing literature on synaptic plasticity and FASD.
  • Analysis of molecular changes affecting neurotransmission, myelination, and neuroinflammation in FASD.
  • Examination of studies identifying immediate and long-lasting synaptic alterations.

Main Results:

  • Prenatal alcohol exposure causes CNS damage, resulting in synaptic structural, functional, and behavioral impairments characteristic of FASD.
  • FASD pathogenesis involves alterations in molecules critical for neurotransmission, myelination, and neuroinflammation.
  • Numerous molecular approaches have identified synaptic changes essential for plasticity and cognitive function in FASD.

Conclusions:

  • Synaptic dysfunction is a key feature of FASD.
  • Understanding synaptic changes in FASD is vital for advancing knowledge and developing therapeutic strategies.
  • Identifying synaptic targets could lead to novel treatments for the neurobehavioral abnormalities associated with FASD.