人类情绪记忆的行为遗传学与神经遗传学研究进展述评

情绪记忆及其增强效应存在广泛的个体差异，这种个体差异可能有其神经与遗传基础。近来的行为遗传学与神经遗传学证实人类ADRA2B基因缺失突变以及BDNF Val66Met基因的多态性与情绪记忆增强及其神经机制的个体差异相联系。本文重点介绍与人类情绪记忆相关的这两种基因，梳理了行为与神经遗传学研究的最新进展，指出未来应关注更多候选基因，并重视多个脑区之间的交互作用；还应使用情绪面孔刺激探索BDNF Val66Met基因多态性对情绪记忆编码和提取的影响等。

Advance of Behavioral Genetics and Neurogenetics of Human Emotional Memory

Lots of studies revealed the effects of emotional memory enhancement, that is, we remembered more emotional arousing events more vividly than neutral events, which has significant adaptive value in evolutionary terms implicated in human survival. However, there are extensive individual variations in emotional memory phenomenon, based on some neural and genetic substrates. Recently behavioral genetics and neurogenetics researches of emotional memory made a great breakthrough and confirmed this hypothesis. Firstly, two sorts of genes were introduced in details in this review--the deletion variant of ADRA2B and BDNF Val66Met polymorphism. Moreover, this review discussed the advances of behavioral genetics and neurogenetics of emotional memory. The first behavioral genetics study (de Quervain et al., 2007) using photographs from the international affective pictures system (IAPS) found that the deletion variant of ADRA2B is related to individual differences in enhanced memory for emotional information in healthy young Swiss participants and increased traumatic memory in Saharan African refugees who experienced multiple and highly aversive life-threatening situations. Specifically, the deletion carriers showed more enhanced short-term emotional memory processes and long-term traumatic memories compared with noncarriers. These data suggested that the deletion variant of ADRA2B acts primarily as a loss-of-function polymorphism of the α2b-adrenergic receptor in the regulation of emotional memory. Based on the first behavioral genetics study, this research group continued to finish a neurogentics study to deeply explore the neural mechanisms of the emotional memory enhancement effects by using pictures from IAPS and event-related functional MRI techniques(Rasch et al., 2009). During encoding negative pictures, carriers of the ADRA2B deletion variant exhibited higher amygdala activation and significant stronger functional connectivity between amygdala and insula compared with noncarriers of the deletion. The findings indicated that the ADRA2B deletion variant is related to increased responsivity and connectivity of brain regions implicated in emotional memory. The latest study confirmed these previous findings and extended that the deletion variant in the ADRA2B gene leads to larger contributions of the amygdala and inferior frontal gyrus to successful formation of emotional memories(Urner et al., 2011). However, a study fine-mapping the genomic region harbouring BDNF and BDNFOS showed a significant association of the SNP rs6265 (Val66Met) with the recall of words with positive emotional content 24 h after learning. Specially, Val/Val homozygous participants had better memory performance than Met carriers. Above all, these behavioral genetics and neurogenetics studies break new grounds in emotional memory research and further support the view that emotional memory system have some specificities, which is largely independent of memory for neutral information. Future studies will focus on more candidate genes and interactions between multiple brain regions. Moreover, it is necessary to use positive and negative arousing face expressions and increase the amount of male participants to investigate how the BDNF Val66Met polymorphism influences the encoding and recognition of emotional face in future. And it seems reasonable to focus on the influences of gene variations and polymorphism on emotional memory trade-offs effects or memory narrowing, not limited in discussion of emotional memory enhancement effects.