as well as heroin and cocaine addiction in humans [61]. Genetic manipulation in PDYN or κ-opioid receptors also supports the importance of this network in regulation of alcohol consumption in mice [62], [63]. Two phosphodiesterases, PDE10A and PDE1B, are part of the network and PDE10A regulates DARP-32 phosphorylation [64]. PDE10A was one of the top PFC genes in a study [10] of individual differences in alcohol drinking in mice and expression of PDE10A is increased by stress, which appears to be important for stress-induced increases in alcohol consumption in rats [65]. Our PFC network is based on changes in expression of 22 genes produced by CI drinking, and five of the genes (including DRD1, PDYN and PPP1R1B) are also changed by Chronic consumption and seven are changed by LPS treatment. For all differentially expressed genes, there was significant overlap between CI and Chronic as well as CI and LPS. CI and LPS share the behavioral feature of increasing alcohol consumption. In view of the representation of some components of the dopamine network in the LPS group, it is important to note that a similar LPS treatment produces a decrease in the firing of brain dopamine neurons [14].
