TY - JOUR
T1 - Estradiol protects against alteration of protein kinase Cε in a binge model of ethanol dependence and withdrawal
AU - Jung, Marianna Eunsun
AU - Jacobs, Stephanie
AU - Rewal, Mridula
AU - Wilson, Andrew
AU - Simpkins, James William
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/5/16
Y1 - 2005/5/16
N2 - 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.
AB - 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.
KW - 17β-estradiol
KW - Ethanol withdrawal
KW - Membrane translocation
KW - Protein kinase Cε
UR - http://www.scopus.com/inward/record.url?scp=20344396118&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2005.03.038
DO - 10.1016/j.ejphar.2005.03.038
M3 - Article
C2 - 15894303
AN - SCOPUS:20344396118
SN - 0014-2999
VL - 515
SP - 62
EP - 72
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1-3
ER -