Human memory is highly influenced by emotion. In healthy subjects events that are emotionally charged—and it doesn’t matter if the emotions are positive or traumatic—tend to be much better remembered than emotionally neutral events. This psychological tendency comes with a glaring exception, however: in some individuals, extremely stressful or traumatic events can induce amnesia, so that they lose the ability to remember what happened. In some instances this loss can lead to the erasure of a vast amount of memory, so that people even forget basic facts about their identity, such as where they live or what their name is.
Amnesia induced by negative emotions is considered a psychological defense mechanism that protects the organism from the consequences of extreme trauma and catastrophic fear. However, recent studies suggest that emotion induced memory loss can also prevent appropriate coping mechanisms, so that people never learn to deal with their painful emotions. (Even if these emotions can’t be recalled, they can still linger below the surface and have psychological consequences.) Hence, understanding how negative emotions induce amnesia, and why only some people who are exposed to traumatic events develop emotion induced amnesia, may have clinical and preventive implications.
The Genetics of Stress
This new study, by the neuroscientist Bryan Strange and colleagues at the Wellcome Trust Center for Neuroimaging in London, examined the role of serotonin transporter genes (5-HTTLPR) in the development of emotion induced amnesia. (Such transporter genes influence the availability of the serotonin transporter, a key regulator of serotonin transmission between brain cells.) Serotonin transporter genes have been extensively investigated for their role in stress induced psychiatric disorders, such as post-traumatic stress disorder (PTSD). In recent years, scientists have found that subjects with 5-HTTLPR short variant genotype are more likely to get depressed after stressful life events and are also at increased risk for PTSD. Furthermore, this short variant genotype is associated with anxiety related traits that have also been implicated in the susceptibility to anxiety and depression.
In the experiment, the authors demonstrate that subjects with the 5-HTTLPR short variant genotype had difficulty remembering a series of neutral words (harvest, kid, thought, and so on) that were presented prior to the presentation of emotionally charged words (such as rape, abortion, tumor), at least when compared with subjects who have the 5-HTTLPR long variant genotype. It’s important to note, however, that these genes did not affect memory for emotional words. Thus, the data suggest that the contribution of 5-HTTLPR to disturbances in emotional memory may be specific to emotion-induced retrograde amnesia, which occurs when subjects are unable to remember what happened before the traumatic event. In contrast, other serotonergic genes, or genes linked with other neurotransmitter systems, might influence memory for emotional words. Based on these experiments, the authors conclude that emotion induced memory is a complex phenomenon influenced by multiple genes. Although serotonin transporter genes may play a role in regulating emotion induced retrograde amnesia, they do not seem to underlie all forms of emotion-induced memory loss.
The Amygdala and Memory
The amygdala is a brain region critical for the experience and expression of emotion as well as for the consolidation of emotional memory. At a modest level of activation, the amygdala seems to augment the function of the hippocampus, a brain region involved in the formation of long-term memory. When the amygdala is greatly excited, as during traumatic events, however, hippocampal function is inhibited and memory impairment is triggered. Other studies have demonstrated that subjects with the 5-HTTLPR short variant genotype have enhanced amygdala reactivity to emotional stimuli. The hyperactive amygdala in these individuals may, at least in part, explain why they are more susceptible to emotion-induced memory loss. This model does not explain why the memory impairment involved is only for the events preceding the negative emotional event and not for the core negative event itself, however.
One potential implication of this research involves preventative genetic testing. By screening high risk subjects for the 5-HTTLPR short variant genotype—including in military personnel or survivors of childhood trauma—doctors and therapists can better focus their energies. In theory it should also be possible to develop medications or cognitive strategies that regulate or suppress the expression of serotonin transporter short variant genes, which should be useful in preventing and treating PTSD or other stress induced psychiatric disorders. Researchers also need functional brain imaging studies to better understand the genetic underpinnings of the relation between amygdala responses to negative stimuli and its interactions with the hippocampus in the manifestation of emotional memory. In conclusion, this paper showing a link between 5-HTTLPR short variant genotype and emotion induced memory loss marks an important advancement in understanding the genetic basis of stress induced psychiatric disorders and sets the stage for personalized mental health care based on risk factors for mental illness.
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