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Synaptic targets: Chronic alcohol actions.

Marisa Roberto1, Florence P Varodayan1

  • 1The Scripps Research Institute, United States.

Neuropharmacology
|January 22, 2017
PubMed
Summary
This summary is machine-generated.

Chronic alcohol exposure alters brain synapses, affecting glutamate and GABA neurotransmission. These neuroadaptations contribute to alcohol dependence and withdrawal symptoms.

Keywords:
Alcohol/ethanolDependenceGABAGlutamateIntoxicationPostsynapticPresynapticProtein phosphorylationSynaptic transmissionTolerance

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Alcohol impacts brain neuronal communication through various molecular targets.
  • Chronic alcohol use and withdrawal induce significant neuroadaptations at synapses.
  • Synaptic changes involve alterations in protein expression, localization, and function.

Purpose of the Study:

  • To review consistent findings on synaptic effects of chronic alcohol exposure.
  • To highlight neuroadaptations contributing to alcohol dependence and withdrawal.
  • To focus on glutamate and GABA neurotransmitter systems.

Main Methods:

  • Literature review of studies on chronic alcohol exposure and synaptic transmission.
  • Focus on consistent and significant neuroadaptive effects.
  • Analysis of effects on major excitatory (glutamate) and inhibitory (GABA) neurotransmitters.

Main Results:

  • Chronic alcohol exposure leads to neuroadaptations in synaptic proteins, channels, and receptors.
  • Altered expression, localization, and function of these synaptic components are observed.
  • Neuroadaptations in glutamate and GABA systems are critical for alcohol reinforcement and dependence.

Conclusions:

  • Synaptic neuroadaptations are central to the development of alcohol dependence.
  • Changes in glutamate and GABA neurotransmission mediate alcohol reinforcement and withdrawal.
  • Understanding these synaptic effects is crucial for addressing alcoholism.