Estradiol protects against alteration of protein kinase Cε in a binge model of ethanol dependence and withdrawal

Marianna Eunsun Jung, Stephanie Jacobs, Mridula Rewal, Andrew Wilson, James William Simpkins

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

This study tested the hypothesis that a binge type of ethanol intake and ethanol withdrawal disturbs protein kinase C (PKC) homeostasis in a manner protected by 17β-estradiol. Ovariectomized rats implanted with 17β-estradiol or oil pellets received ethanol (7.5% weight/volume, 7 days) or control solution by a gavage method. The cerebelli were collected during ethanol exposure or ethanol withdrawal to assess the activity, protein levels, and cellular distribution of PKCε and total PKC, using an ATP phosphorylation and immunoblot assays. While both ethanol exposure and ethanol withdrawal increased membrane protein levels and membrane translocation, only ethanol withdrawal enhanced activity of PKCε. Ethanol withdrawal not ethanol exposure increased the three parameters of total PKC. 17β-Estradiol treatment prevented these changes in PKC profiles. These data suggest that an excessive episodic intake of ethanol followed by ethanol withdrawal disturbs PKC homeostasis and cellular distribution of PKC, in particular PKCε, in a manner that is protected by estrogen. PKCε appears more vulnerable during ethanol withdrawal than during ethanol exposure.

Original languageEnglish
Pages (from-to)62-72
Number of pages11
JournalEuropean Journal of Pharmacology
Volume515
Issue number1-3
DOIs
StatePublished - 16 May 2005

Keywords

  • 17β-estradiol
  • Ethanol withdrawal
  • Membrane translocation
  • Protein kinase Cε

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