Animal research has begun to provide insight into the molecular mechanisms that underlie resilience. One series of studies has focused on the ventral tegmental area (VTA)-nucleus accumbens reward circuit. In the social defeat stress model40,41 (see Supplementary information S1 (box)) resilience, among a population of inbred (genetically identical) mice, is associated not only with the absence of many of the changes in gene expression that are seen in the VTA-nucleus accumbens of vulnerable mice, but also with the induction of distinct changes in gene expression that occur in resilient mice only41. These findings underscore the view that resilience is not simply the absence of maladaptive changes that occur in vulnerable individuals; rather, it is mediated by a unique set of adaptive changes. As just one example, chronic defeat stress induces in resilient mice the expression of several K+ channel subunits in VTA dopamine neurons, which prevents the stress-induced increase in VTA excitability and the consequent release of BDNF onto the nucleus accumbens — maladaptations that contribute to vulnerability41,67 (FIG. 2). The transcriptional regulation of dozens of additional genes in the
