dependence symptoms in the presence of CSA exposure. This alludes to the potential buffering effects of the A allele in rs604300 on the pathogenic effects of CSA. This is highly congruent not only with one prior study of eCB genotypes and their interplay with childhood trauma to predict anhedonia (Agrawal, Nelson, et al., 2012), but also complies with observations in rodent paradigms documenting the role of eCBs in stress adaptation (e.g., Gunduz-Cinar, MacPherson, et al., 2013; Hill & Gorzalka, 2006; Hill & McEwen, 2010; Hill, Patel, et al., 2010; Patel, Roelke, Rademacher, Cullinan, & Hillard, 2004; Viveros, Marco, & File, 2005). Importantly, our finding of increased amygdala habituation as a function of ELS in minor A allele carriers, but not in GG individuals, reinforces the possibility that MGLL rs604300 genotype may play a key role in decoupling the neurobiological link between ELS and mental health outcomes in later life. Such increased amygdala habituation to threatening stimuli may be reflective of an adaptive response that could potentially promote fear extinction when a threat is no longer imminent and, speculatively, a decreased reliance on substances for affect regulation. In support of this hypothesis, a post-hoc SEM demonstrated that the pathway from CSA
