Understanding genetic contributions to individual differences in the capacity for emotional memory has tremendous implications for understanding normal human memory as well as pathological reactions to traumatic stress. Research in the last decade has identified genetic polymorphisms thought to influence cognitive/affective processes that may contribute to emotional memory capacity. In this paper, we review key polymorphisms linked to emotional and mnemonic processing and their influence on neuromodulator activity in the amygdala and other emotion-related structures. We discuss their potential roles in specific cognitive processes involved in memory formation, and review links between these genetic variants, brain activation, and specific patterns of attention, perception, and memory consolidation that may be linked to individual differences in memory vividness. Finally we propose a model predicting an influence of noradrenergic, serotonergic, and dopaminergic processes on emotional perception, as well as on memory consolidation and self-regulation. Outside of the laboratory, it is likely that real-life effects of arousal operate along a continuum that incorporates other "non-emotional" aspects of memory. For this reason we further discuss additional literature on genetic variations that influence general episodic memory processes, rather than being specific to emotional enhancement of memory. We conclude that specific neuromodulators contribute to an amygdala-driven memory system that is relatively involuntary, embodied, and sensorily vivid.
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