Influence of COMT val158met and ADRA2B deletion polymorphisms on recollection and familiarity components of human emotional memory.

Emotional enhancement of memory is a widely accepted phenomenon that, in addition to its adaptive role, may play a role in the evolution of psychiatric disorders. Hence a comprehensive understanding of its neurobiological basis is imperative. Whilst the pharmacological and neural mechanisms are well known, the contribution of genetic variation is not. Research suggests that two qualitatively different processes (recollection and familiarity) contribute to recognition memory. In this study, we examined the relative contribution of two common genetic polymorphisms, the deletion variant of the ADRA2B gene that codes the α2b adrenergic receptor and the val158met polymorphism of the COMT gene that codes the catechol-O-methyltransferase enzyme, to emotional enhancement of these two memory processes in 97 healthy male volunteers. There was a significant interaction between COMT genotype and emotional arousal in relation to recollection, but not familiarity, with the former being significantly elevated for emotionally arousing versus neutral pictures in carriers of the val158 allele compared with met158 carriers. There were no main effects or interactions in relation to ADRA2B genotype.

Effects of amisulpride on emotional memory using a dual-process model in healthy male volunteers.

Memory dysfunction occurs in a number of neuropsychiatric disorders. Therapeutic psychopharmacological agents may exacerbate such memory impairment. Detailed characterisation of drug-induced memory impairment is therefore important. We recently showed that the D(2)/D(3) antagonist amisulpride quantitatively impairs emotional memory in a randomised placebo-controlled study of 33 healthy volunteers. Current evidence suggests that two qualitatively different processes (recollection and familiarity) contribute to recognition memory and can be investigated using a Dual-Process Signal Detection model. Using such a model, we found that amisulpride levels at encoding were significantly inversely correlated with recollection estimates for emotional but not neutral stimuli or familiarity estimates in healthy male volunteers. This suggests that dopamine antagonism at encoding preferentially impairs the recollection component of emotional memory, relative to the familiarity component. This was supported by receiver operating characteristic analysis. We also found a significantly increased false recognition rate, associated with significantly shorter reaction times for emotional but not neutral stimuli in the amisulpride group. These findings have important implications for our understanding of recognition memory processes, as well as the interpretation of neuropsychological findings in medicated patients.