The neurogenetics of traumatic memories


It is well known that traumatic memories, or those with other emotional significance, are more persistent than trivial or mundane ones. The death of a loved one, for example, is far more readily recalled than an uneventful car journey to work.

Evolutionarily, enhanced memory of a highly emotional event – say, a situation when one’s life is in danger – is an advantage, because that information will be potentially life-saving if that situation is encountered again. But persistent memories of such events can have adverse effects, as they can lead to conditions such as post-traumatic stress disorder (PTSD).

Now, a new study led by Dominique de Quervain, a psychiatrist at the University of Zurich, shows that the enhanced ability to recall emotional memories is associated with a mutation in a gene encoding a neurotransmitter receptor. The findings could eventually lead to new treatments for PTSD and other anxiety disorders.

Emotional memories are encoded in the amygdala, a small, almond-shaped structure found deep in the brain on the medial (inner) surface of the temporal lobe. The amygdala forms connections with other regions of the brain that are involved in memory consolidation, such as the hippocampus.

From previous studies, it is known that certain types of noradrenaline receptors (adrenoceptors) are involved in the formation of emotional memories. For example, blocking alpha-adrenoceptors by injecting the drug yohimbine directly into the amygdala of mice increases the effects of emotional arousal on memory consolidation.

One subtype of adrenoceptor that has been implicated in this process is the alpha2b-adrenoceptor, which is encoded by the ADRA2B gene. In the amygdala, this receptor has a modulatory function – it indirectly inhibits the release of noradrenaline by activating specific biochemical pathways. 

A second and less common form of the gene has 3 amino acids missing. Because this deletion variant of the ADRA2B encodes a protein whose function is impaired, the authors of the new study speculated that it might be related to individual differences in the ability to recall emotional information.

To test their hypothesis, they recruited 435 Swiss students, and asked them to perform a memory test in which they were presented with a series of 30 photographs. 10 of the images were positive (e.g. children playing), 10 were negative (e.g. car accidents), and the remaining 10 were emotionally neutral.

The participants were asked to rate the emotional content of each photograph immediately after it was shown to them. 10 minutes later, they were asked to recall the photographs and describe each using a few words.

It was found that all participants recalled the photographs with emotional content – both positive and negative – more accurately than the neutral images. But, more importantly, those participants carrying either one or two copies of the deletion variant recalled the emotionally charged images even more accurately than the non-carriers.

As there was no significant difference between how carriers and non-carriers rated the positive and negative photographs the authors conclude that the gene variant affects the consolidation of emotional memories and not the level of the emotional response to the images.

Because enhanced consolidation of emotional memories often leads to disturbing “re-experiences” of traumatic events, the authors further hypothesized that carriers of the deletion variant gene would be more susceptible to distressing recall of traumas they had experienced in the past.

To determine whether or not this was the cse, the researchers then travelled to Nakivale refugee camp in Uganda, home to hundreds of refugees who fled the Rwandan civil war of 1994.

With the help of specially trained interviewers from within the refugee community, they tried to determine the extent to which the 202 refugees who took part in the study had suffered flashbacks of the traumatic events they had experienced.

The Rwandan civil war was an extremely brutal conflict, in which 1 million Rwandans were killed in the space of a few months. All of the 202 had therefore experienced and witnessed multiple traumatic events, such as mutilation and rape.

In confirmation of their hypothesis, the researchers found that those refugees who carried the deletion variant reported having significantly more re-experiences of the traumatic events from the past than non-carriers.

However, the association between the deletion variant of the adrenoceptor gene and enhanced memory consolidation was independent of the presence of PTSD in the refugees studied. Nevertheless, noradrenergic receptors are a potential target for pharmacological treatments for PTSD and other similar disorders.   

Exactly how the alpha2b-adrenoceptor leads to enhanced memory consolidation is unclear. But the receptor normally functions to inhibit noradrenaline release in the brain, so it seems likely that the deletion leads to an inhibition of this inhibition. Thus, inhibition of this inhibition would lead to increased noradrenaline release in the amygdala during a stressful event, making the memory of that event stronger. 


de Quervain, D. J-F., et al. (2007). A deletion of the alpha2b-adrenoceptor is related to emotional memory in Europeans and Africans. Nat. Neurosci. doi: 10.1038/nn1945. [Abstract]



2 thoughts on “The neurogenetics of traumatic memories

  1. Bravo Mo.
    I may not learn anything on a given day from much of the net. But I have a great chance that I will learn something from Mo’s site.

  2. Thanks for this. Very interesting, especially this:
    “[T]he association between the deletion variant of the adrenoceptor gene and enhanced memory consolidation was independent of the presence of PTSD,…”
    Which kinda confounds the situation a bit.

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