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INTRODUCTION: Matrix metalloprotease 9 (MMP-9) is an extracellularly operating protease shown to play the key role in the morphological reorganization of dendritic spines as well as specific forms of learning and memory. Here we focus on a pathological form of plasticity - synaptic plasticity of alcohol addiction. AIM(S): The aim of this study was to investigate the role of MMP-9 in functional and structural synaptic plasticity during development of alcohol addiction. METHOD(S): Mice, housed in the IntelliCage system, were constantly monitored for alcohol consumption and motivation to reward. Spine morphology was evaluated by confocal imaging. We then performed whole-cell patch clamp recordings to test the strength of synapses as well as formation of silent synapses in the central amygdala. RESULTS: MMP-9 KO mice display lower motivation towards ethanol compared to wild type mice (WT). Moreover, in central amygdala, chronic alcohol drinking produced alterations in dendritic spine shape of both WT and KO but interestingly, more pronounced changes were observed in WT high alcohol consumers. To test how altered structural plasticity affects functionality of synaptic connections, we performed electrophysiological analysis of the strength of glutamatergic synapses in central amygdala. We discovered that alcohol consumption elevates the number of silent synapses (neonatal-like, immature synapses considered as substrates for increased plasticity). MMP-9 KO mice, however, showed no such synaptic adaptations neither after alcohol drinking nor subsequent withdrawal. CONCLUSIONS: These data suggest that MMP-9 is involved in synaptic plasticity associated with alcohol addiction. The change of spine morphology together with elevated silent synapse number might represent ongoing circuitry reorganization that primes neurons for enhanced learning, which might lead to compulsive ethanol use. FINANCIAL SUPPORT: This study is supported by the National Science Centre grant Sonata (2015/19/D/ NZ4/03701).