Scientists from Northwestern University in Chicago have discovered that the brain adopts a process called “state-dependent learning” to bury traumatic memories. The study, done in mice, revealed that stimulating extra-synaptic Gamma-aminobutyric acid (GABA_A) receptors conditioned the mice to fear response, indicating the involvement of this receptor in traumatic memory coding. GABA acts as a neurotransmitter and works to calm the nerves.

The brain tries to shield an individual from traumatic memories such as childhood abuse or any disturbing experience. A so-called  “amnesia” develops so that the individual is unable to access the pain and emotional upheaval associated with a particular traumatic experience.

The interplay between two amino acids, glutamate and GABA, determines the state of the brain, dictating whether the neurons become excited or stay calm. Glutamate keeps the memories fresh and is the amino acid that increases when we are in an excited or alert state. GABA, on the other hand, works to calm our nerves. Both amino acids work with their respective receptors to bring about the desired results. GABA has two kinds of receptors, the synaptic and extra-synaptic. It is the synaptic GABA receptor that works in tandem with glutamate receptors to balance the brain’s reaction to any event.

The extrasynaptic GABA receptor is not affected by glutamate or its receptors. Scientists in the current study treated mice with a drug (gaboxadol) that stimulates extrasynaptic GABA receptors. Both untreated and treated mice were given mild electric shocks after placing them in a particular box. The next day, both were returned to the box. The observations were:

• Gaboxadol untreated mice behaved normally and weren’t afraid.
  
• Gaboxadol treated mice were scared, expecting another electric shock.
  
• The drug treated mice used an entirely different pathway to code the traumatic memory when compared to control mice.
  
• This coding is regulated by a small microRNA, miR-33.

The scientists believe that miR-33 may be the protective mechanism for the brain when it is exposed to traumatic events.

The senior author of the publication, Dr. Jelena Radulovic says in the Public Release of the American Association for the Advancement of Science, "The findings show there are multiple pathways to storage of fear-inducing memories, and we identified an important one for fear-related memories. This could eventually lead to new treatments for patients with psychiatric disorders for whom conscious access to their traumatic memories is needed if they are to recover."

Dr. Radulovic adds, "The brain functions in different states, much like a radio operates at AM and FM frequency bands. It's as if the brain is normally tuned to FM stations to access memories, but needs to be tuned to AM stations to access subconscious memories. If a traumatic event occurs when these extrasynaptic GABA receptors are activated, the memory of this event cannot be accessed unless these receptors are activated once again, essentially tuning the brain into the AM stations."

Written by Mangala Sarkar, Ph.D.

Primary References

Jovasevic, V., Corcoran, K., Leaderbrand, K., Yamawaki, N., Guedea, A., Chen, H., . . . Radulovic, J. (2015). GABAergic mechanisms regulated by miR-33 encode state-dependent fear. Nature Neuroscience. Retrieved August 24, 2015, from http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.4084.html

How traumatic memories hide in the brain, and how to retrieve them. (n.d.). Retrieved August 24, 2015, from http://www.eurekalert.org/pub_releases/2015-08/nu-htm081415.php

Additional Reference

Dissociative Amnesia | Center for Behavioral Health | Cleveland Clinic. (n.d.). Retrieved August 24, 2015, from http://my.clevelandclinic.org/services/neurological_institute/center-for-behavorial-health/disease-conditions/hic-dissociative-amnesia