Abstract
The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCe is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCe expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCe expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCe to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCe, ethanol-induced changes in PKCe expression, the regulation of ethanol-induced PKCe activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCe-RACKe translocation in the presence of ethanol, and the existing literature on the role of PKCe in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.
| Original language | English |
|---|---|
| Article number | 244 |
| Journal | Frontiers in Neuroscience |
| Volume | 12 |
| Issue number | APR |
| DOIs | |
| Publication status | Published - 12 Apr 2018 |
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Keywords
- Alcohol
- Epsilon
- Ethanol
- PKC
- PKCe
- RACK
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Ethanol-induced changes in PKCe : From cell to behavior. / Pakri Mohamed, Rashidi Mohamed; Mokhtar, Mohd H.; Yap, Sze Wei; Hanim, Athirah; Abdul Wahab, Norhazlina; Farah Hanan Fathihah, Jaffar; Kumar, Jaya.
In: Frontiers in Neuroscience, Vol. 12, No. APR, 244, 12.04.2018.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Ethanol-induced changes in PKCe
T2 - From cell to behavior
AU - Pakri Mohamed, Rashidi Mohamed
AU - Mokhtar, Mohd H.
AU - Yap, Sze Wei
AU - Hanim, Athirah
AU - Abdul Wahab, Norhazlina
AU - Farah Hanan Fathihah, Jaffar
AU - Kumar, Jaya
PY - 2018/4/12
Y1 - 2018/4/12
N2 - The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCe is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCe expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCe expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCe to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCe, ethanol-induced changes in PKCe expression, the regulation of ethanol-induced PKCe activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCe-RACKe translocation in the presence of ethanol, and the existing literature on the role of PKCe in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.
AB - The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCe is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCe expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCe expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCe to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCe, ethanol-induced changes in PKCe expression, the regulation of ethanol-induced PKCe activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCe-RACKe translocation in the presence of ethanol, and the existing literature on the role of PKCe in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.
KW - Alcohol
KW - Epsilon
KW - Ethanol
KW - PKC
KW - PKCe
KW - RACK
UR - http://www.scopus.com/inward/record.url?scp=85046086159&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85046086159&partnerID=8YFLogxK
U2 - 10.3389/fnins.2018.00244
DO - 10.3389/fnins.2018.00244
M3 - Review article
AN - SCOPUS:85046086159
VL - 12
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
SN - 1662-4548
IS - APR
M1 - 244
ER -