Alcohol addiction is a chronic, psychiatric disease defined by compulsive alcohol drinking and seeking. Long-term alcohol intake induces aberrant synaptic plasticity in the amygdala and striatum as well as enhanced c-Fos expression in the central nucleus of amygdala (CeAmy). Interestingly, human studies have implicated matrix metalloproteinase 9 (MMP-9), whose gene is regulated by c-Fos, in alcohol addiction. Notably, recently critical role of MMP-9 in reward-driven learning as well as synaptic plasticity has been revealed. In the present study we aimed at elucidating a role of MMP-9 in alcohol addiction in mice. First, we analyzed the effects of MMP-9 levels on the dendritic spine morphology in the CeAmy of C57BL/6 wild type (WT) and mice lacking MMP-9 (MMP-9 KO). Next, to verify the role of MMP-9 in alcohol addiction we subjected WT, MMP-9 KO and heterozygous mice to behavioral tests in the Intellicage system, previously shown to be suitable to investigated addictive behaviors. Dendritic spine analysis of the CeAmy revealed that MMP-9 KO mice have longer and thinner dendritic spines than WT mice. Preliminary data analysis from the Intellicages showed there were no differences between MMP-9-KO and WT mice during first hour and first day activity, as well as in neophobia. Currently we are investigating the pattern of development of the alcohol addiction, to evaluate the role of MMP-9 in aversive aspects of this behavior.
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