A new study from Uppsala University in Sweden has shined light on the emotions involved with fear and its memory recall. Published on Sept. 20 in the journal Science, researchers indicate that it is possible to remove a fear-inducing memory by activating the fear followed by a disruption during a period known as “reconsolidation interval.” This added disruption is able to erase the developed fear memory from the amygdala in the brain. As the study states, “this mechanism holds great clinical promise in anxiety treatment in order to dissociate fear from cognitive memory.”

The amygdala is a set of neurons that is located in an area of the brain known as the temporal lobe. Involved in the processing of emotions such as fear, anger, and pleasure, the amygdala also plays a function in determining what and where memories are stored in the brain. This ability to store memories ultimately leads to the inclusion of linking stressful events to previously neutral stimuli, which leads a person to become fearful.

Using a sample of 11 men and 11 women, researchers established a fear memory by giving a shock along with a cue. After the fear was established within the subjects, the study randomly assigned the subjects to two different groups: disruption during this reconsolidation interval and disruption after the reconsolidation interval. The study proved that subjects that received disruption during the reconsolidation period were able to eliminate the fear memory in the amygdala. The subjects that received disruption outside the interval had a recall of the fear stimulus.

“By activating memories and disrupting their reconsolidation, through protein synthesis blockade localized in the amygdala or through systematic administration of beta-adrenergic receptor antagonists, fear memories are inhibited,” noted researchers.

The knowledge gained from this study may help to reduce stress in patients in a more natural way. While pharmaceuticals are available to treat these forms of anxiety, they can only work so well, as relapses of the fear memory may result in a sudden and unexpected regression.

A new study, published by the online journal Current Biology on Sept. 20 has deciphered the physiological concept behind compulsive over-consumption. By performing microinjections in the brains of lab rats, researchers were able to conclude that the anteromedial quadrant of the dorsal neostriatum of the brain generates motivation to over-consume. This motivation may help to explain nonstandard behaviours in humans such as binge eating and drug addiction.

With lab rats as its subjects, the researchers injected “mu opiod stimulation” through a polypeptide known as enkephalin. This was introduced into the anteromedial quadrant dorsal neostriatum of its brain. Using M&Ms as its testing material, the injection of enkephalin proved effective as the rats ate a significant amount more chocolates than the control group. It was noted that most rats ate at least 17 grams of M&Ms, equivalent to roughly five per cent of their body weight. As the study notes, “That level of elevated consumption is roughly proportional to a 68kg human consuming [approx.] 3.6 kg of M&Ms in a single hour.”

The study was also able to deduce that while this micro-injection was able to stimulate an “eat now” command, it should not be confused with subjects increasing their “likeness” toward the M&Ms. This concept can also be noted in drug addicts, who may not necessarily “like” the drug they are taking but continue to consume because of this mu opoid stimulation.

While past studies have tried to understand the physiological concept behind overconsumption with little success, DiFeliceantonio et al. note that these studies did not distinguish the four quadrants of the dorsal neostriatum of the brain. The motivation that caused the rats to eat more M&Ms only occurred when mu opoid stimulation was injected into the anteromedial quadrant.