In particular, although the “Signal transduction” category has been consistently identified across studies, distinct signaling pathways were affected depending on the conditions of exposure. The mitogen-activated protein kinase (MAPK) cascade was identified in rodent models of differential ethanol consumption [38, 51] and following chronic ethanol exposure [30, 32, 52, 53]. Retinoic acid signaling was altered by acute and chronic ethanol treatment, as well as in alcoholics [53-55]. Rats with differential ethanol preference showed innate differences in small GTPase-mediated signal transduction, as did mice exposed to acute ethanol [48, 56]. Glucocorticoid signaling was altered following acute or chronic ethanol exposure [25, 54] and some of the transcriptional changes induced by acute ethanol exposure were reversed by an antagonist of the glucocorticoid receptor [48]. Chronic ethanol exposure, drinking or abuse affected the cAMP/PKA [32, 55], phosphoinositide 3-kinase [32, 53], calcium [25, 52, 55], and thyroid hormone [35, 55] signaling pathways. The notch and Janus kinase/signal transducers and activators of transcription (JAK/STAT) cascades were identified in individual studies using chronic ethanol exposure [30, 53]. In addition, a study focusing on a collection of
