Researchers have found that a mutation in the ADRA2B gene improves the recall of emotional memory. This specific mutation of ADRA2B deletes three amino acids from the encoded protein. This mutation affects the behavior of noradrenaline receptors.

The research team tested this gene mutation by genotyping 435 young adults. These participants were shown a series of pictures. The pictures were one of three emotional categories: neutral, positive and negative. After viewing all the pictures for 4 seconds each, participants were asked to write a description of what they had seen. Participants with the ADRA2B mutation recalled up to 80% of the emotional images while those without the mutation recalled on average 40%.

The team believes the mutation is as common as 30% in Caucasians and 12% in Africans. The study also contacted people suffering from Post-dramatic Stress Disorder. Those with the mutation recalled their negative emotional memories more vividly than those without the mutation.

On the flip side, Retrospectacle recently posted an interesting article on a new drug, propranolol, which “blocks the action of epinephrine on both β1- and β2-adrenergic receptors”. The drug weakens and removes emotional attachment to past memories. Participants are asked to vividly recall their traumatic memory and are then administered the drug. I would theorize that recalling a memory is somewhat similar pharmacologically to experiencing it the first time and thus the beta-blocking capabilities of propranolol minimizes the “resaving” of the memory. Of course, this is wild speculation and I have zero direct evidence to support my theory

It is believed that propranolol works because of the interaction between norepinephrine and glucocorticoids. Glucocorticoids are released by the adrenal cortex during emotional arousal and are believed to consolodate and strengthen new memories. It was theorized that glucocorticoid release was triggered by norepinephrine.

To test this, mice were trained with an object recognition task and received a placebo solution or corticosterone, either alone or with propranolol. The mice were given three minutes to familiarize themselves with an object in their environment. After this training they were administered their cocktail of drugs. After 24 hours, the mice were exposed to a new object identical to the first one. The mice that received the placebo showed no special interest in the new object. The mice that had received corticosterone post-training, however, showed significant preference to the new object. Mice that received propranolol alone or both propranolol and corticosterone showed similar results to those that received a placebo solution. This trial suggests that corticosterone increases object recognition of objects and that the co-administration of propranolol removed that effect.

Another trial attempted to find a similar relationship in mice that had already been exposed to the object recognition task previously. Mice that had already been habituated to the object recognition task did not show an increase in norepinephrine levels due to a novel environment and therefore did not respond to corticosterone administration. The trial therefore artificially stimulated norepinephrine levels with yohimbine. The same object recognition training was done as before. Mice receiving only corticosterone or only yohimbine did not show increased object recognition. Mice receiving both concurrently, however, showed an increased recognition on a dose-dependent basis.

The study showed that corticosterone enhanced object recognition when adminstered after a norepineprhine release due to the addition of a novel object. Artificially stimulating norepinephrine also enabled corticosterone to increase object recognition when it would not normally because of pre-exposure to the training. Furthermore, administration of propranolol blocked the increased object recognition traits granted by corticosterone administration. The study strongly suggests that both systems, norepinephrine and corticosterone release, must be triggered at the same time for emotional memory storage. When one of them is blocked, as in the case of propranolol, emotional memory is not stored. Also very important, the study demonstrated that corticosterone release was not triggered by norepinephrine, as previously thought. They are, infact, two separate systems that must occur at the same time.