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Ethanol tolerance and synaptic plasticity

L J Chandler1, R A Harris, F T Crews

  • 1Department of Pharmacology and Therapeutics, Louisiana State University Medical Center, Shreveport 71130, USA.

Trends in Pharmacological Sciences
|January 1, 1999
PubMed
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Ethanol disrupts central nervous system (CNS) ion channel function, leading to tolerance and dependence. Adaptive synaptic changes, including modifications to NMDA and GABAA receptors, likely underlie these effects.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Ethanol's central nervous system (CNS) effects are linked to ion channel disruption.
  • Understanding ethanol tolerance and dependence is crucial for clinical management.
  • Synaptic function adaptations are implicated in ethanol's long-term effects.

Purpose of the Study:

  • To explore mechanisms of ethanol-induced synaptic function changes.
  • To provide a cellular basis for ethanol tolerance and dependence.
  • To discuss the roles of NMDA and GABAA receptors in these adaptations.

Main Methods:

  • Review of current concepts on ethanol's interaction with ion channels.
  • Discussion of potential transcriptional and post-translational modifications.

Related Experiment Videos

  • Analysis of receptor subunit protein interactions.

    • Main Results:

    • Ethanol interacts with hydrophobic sites on ion channel proteins.
    • Adaptive synaptic changes contribute to ethanol tolerance and dependence.
    • Both NMDA and GABAA receptors are likely targets for ethanol-induced modifications.

    Conclusions:

    • Multiple mechanisms, including transcriptional and post-translational modifications, underlie ethanol's effects on synaptic function.
    • These modifications in NMDA and GABAA receptors offer a cellular explanation for ethanol tolerance and dependence.