Genome-wide analysis of ethanol-responsive genes has been the subject of intense research during the past decade. Microarray analysis of cultured neural cells (SH-SY5Y neuroblastoma cells) showed that ethanol exposure altered the expression of genes involved in cyclic AMP (cAMP)/protein kinase A (PKA) signaling and norepinephrine production, as well as in oxidative stress and protein synthesis [14, 15]. In the nematode, ethanol exposure rapidly induced a cellular stress response (heat shock protein genes) [16]. Gene profiling in the fruit fly also identified ethanol-responsive gene sets associated with stress response, along with olfaction, metabolism, transcription and signal transduction [17]. The present review focuses on whole-genome expression profiling in rodent genetic models of differential ethanol sensitivity or consumption, in rodents acutely or chronically exposed to ethanol and in human alcoholics. Importantly, rodent models and postmortem brain tissue have their own limitations and provide complementary biological information. While no animal paradigm can fully replicate the complexity of alcoholism, validated models enable the dissection of specific aspects of the syndrome with a tight control over experimental conditions and the possibility to use large numbers of
