Ethanol consumption and behavioral impulsivity are increased in protein kinase C gamma null mutant mice

Citation
Bj. Bowers et Jm. Wehner, Ethanol consumption and behavioral impulsivity are increased in protein kinase C gamma null mutant mice, J NEUROSC, 21(21), 2001, pp. NIL_12-NIL_16
Citations number
37
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE
ISSN journal
02706474 → ACNP
Volume
21
Issue
21
Year of publication
2001
Pages
NIL_12 - NIL_16
Database
ISI
SICI code
0270-6474(20011101)21:21<NIL_12:ECABIA>2.0.ZU;2-G
Abstract
Etiological factors influencing the development of alcoholism are complex a nd, at a minimum, include an interaction between polygenic factors and pers onality and biological traits. Human and animal studies suggest that some g enes may regulate both the traits associated with alcohol abuse, such as de creased sensitivity or anxiety, and vulnerability to alcoholism. The identi fication of these genes could elucidate neurochemical pathways that are imp ortant in the development of alcohol abuse. Results from the present study indicate that the gene encoding the neuronal-specific gamma subtype of prot ein kinase C (PKC gamma) influences both ethanol consumption and behavioral impulsivity, a personality characteristic associated with Type II alcoholi cs, in a pleiotropic manner. Mice lacking PKC gamma consume more ethanol in a two-bottle choice paradigm and also demonstrate increased behavioral imp ulsivity in an appetitive-signaled nose-poke task when compared with wild-t ype littermate control mice. Therefore, PKC gamma may be an important mecha nism within the cell that mediates one or more neurochemical pathways relev ant to an increased predisposition to alcoholism.