What really goes on in your brain when you experience a stressful event? And the memories that are formed, what makes them shift from a helpful reminder of a trepidatious situation to a triggering event? These are questions that neuroscientists are asking about memories formed after stressful events. While it seems obvious that stress is a part of human life and remembering past events contributes to learning and success in our futures, there are some stressful events that create memories upon whose recall manifests as anxiety or PTSD symptoms. Are these memories a coping mechanism for dealing with extreme stress and trauma, or do they exacerbate the trauma such that it adversely affects someone’s life experience long after the fact?
The molecular pathway outlined in Reul’s article involves a stress hormone stimulus that causes a protein to be modified in such a way that it allows two genes to be transcribed. These genes code for proteins that are important for the growth of neurons and memory consolidation. In a stressful situation, these genes are transcribed in higher amounts, allowing for a stressful event to be recorded and remembered in the brain. If a more anxious person experiences a stressful event, more proteins are synthesized, and the memory consolidation is stronger.
Here are three proposed molecular differences in brains that experience stressful events and develop stress-related disorders and brains that do not:
- Epigenetics: the differing expression of genes related to external stimulation. Genetic predisposition to stress-related disorders (including PTSD and general anxiety) are implicated in studies showing that the same stressful experiences are recorded differently in the brain. While many people experience extreme stress in their lives, only between 10-20% of them develop a stress-related disorder.[1]
- GABA: the brain’s primary inhibitory neurotransmitter. When a lot of GABA is present in the dentate gyrus, there is less of an anxious response to a stressful situation: the molecular pathway outlined above is inhibited. Congruently, increased excitability of neurons leads to higher expression of memory consolidation genes.
- Hippocampus: the emotion processor involved with memory formation. A region of the hippocampus is important for the integration of emotional and cognitive data. When this area is functioning improperly, learning and memory are impaired. Additionally, the interplay between this region and the amygdala leads to decreased memory storage in the dentate gyrus. The lack of memory formation would directly affect the chance that someone who experiences a stressful event would remember it or develop a stress-related disorder.
It’s definitely a tricky situation with lots of interplay between genetic make-up, individual environment, and so many other factors that we as scientists do not understand and we as humans simply have to live with and help each other to live with.
[1] Reul, Johannes M.J.M. 2014. Making memories of stressful events: a journey along epigenetic, gene transcription, and signaling pathways. Frontiers in Psychiatry 5(5):1-11.
