PPARs are nuclear hormone receptors that act as ligand-activated transcription factors. PPAR agonists are anti-inflammatory, neuroprotective, hepatoprotective and have anti-addictive properties 9, 15, 39, 59. Little is known about the mechanisms underlying their CNS effects; thus, we used an unbiased genomic approach to characterize expression profiles in amygdala and PFC by two PPAR agonist treatments that are effective (feno and tesa), and one that is not effective (beza), in reducing alcohol consumption. The transcriptomes were examined using several bioinformatic approaches, including differential expression analysis and WGCNA. All transcripts were analyzed simultaneously, providing a detailed molecular phenotype of brain responses following activation of the PPAR signaling pathway. A dataset of expression levels for most genes in the mouse genome has been made publicly available in Gene Expression Omnibus. This profile will also aid researchers studying other brain diseases that are responsive to PPAR agonists (Alzheimer’s, Parkinson’s, and Huntington’s disease, ischemic brain injury, and schizophrenia), and help define neural mechanisms (and therefore potential treatment) of several CNS diseases.
