Having a hard time recalling where you put those tax forms? Blame it on stress.
Using animal models, ASU professor and researcher Cheryl ConradIn addition to her position as a professor and researcher of behavioral neuroscience in ASU’s Department of Psychology in the College of Liberal Arts and Sciences, Conrad serves as assistant vice president of research development for ASU’s Knowledge Enterprise Development. has found that chronic stress can impair certain cognitive functions of the brain.
“[Animals] have a robust stress response and a lot of similarities to changes that we see in people,” she said.
Better understanding the mechanisms behind stress can enable healthier lives by combating such conditions as depression and PTSD, Conrad said.
One of the functions she has found to be affected by chronic stress is spatial navigation, or the ability to navigate one’s environment based on the memory of landmarks.
Along with grad student researchers Jessica Judd and Bryce Ortiz, she performed an experiment in which rats are placed in a maze with three different corridors to explore. The walls of the room in which the maze is placed are painted with visual cues, such as dots or stripes. The visual cues serve as landmarks to help the rats remember which corridors are located where (similar to how an ASU student knows which mall they are on based on the location of the Memorial Union).
The rat is placed in the maze two separate times. The first time, one corridor is blocked off. The rat is allowed to explore for a set amount of time, then taken out of the maze for a set amount of time. Later, the rat is placed back in the maze with the corridor now unblocked.
Rats have an innate desire to explore new things, so the expectation is that when placed back in the maze with the previously blocked-off corridor now unblocked, they will show more interest in exploring that corridor.
And that proved to be true — for healthy, unstressed rats.
However, rats that were under stress at the start of the experiment showed no increased interest in exploring the now-unblocked corridor, suggesting they did not realize it was new and different.
These findings suggest that stress impairs the ability to navigate based on memory; because the rat was stressed, it did not remember that the now-unblocked corridor was previously blocked, and therefore showed it no more attention than the other two corridors.
The good news is that once the stress ended, so did the impairment of spatial navigation.
What that means, explained Conrad, is that not only is there “no permanent detrimental damage [from chronic stress],” but that “there is an active mechanism in the brain that facilitates the recovery.”
Identifying that mechanism could potentially lead to the discovery of ways in which we can intervene to help in the recovery from chronic stress. Ortiz wrote about the findings in a 2014 paper published in the European Journal of Neuroscience, “Hippocampal brain-derived neurotrophic factor mediates recovery from chronic stress-induced spatial reference memory deficits.”
While the impairment of spatial navigation points to how chronic stress affects the area of the brain known as the hippocampus — which is important for processing facts associated with memories — Judd is looking at how chronic stress affects the area of the brain known as the amygdala, which is important for processing emotions associated with memories.
For people who have experienced traumatic events, certain cues can trigger memories of the event that result in an extreme emotional response, causing them to feel as if they are experiencing the event all over again. This is perhaps most commonly seen among veterans of war, and it is known as post-traumatic stress disorder, or PTSD.
Judd is hoping to identify a way to discriminate between a neutral memory cue and a memory cue that triggers an extreme emotional response to a perceived impending negative event. Doing so would allow researchers to pinpoint the protein that causes the extreme emotional response, and then — it is hoped — block it.
“The idea is that we would go in [to the brain] and modify the protein expression in the amygdala to try to attenuate a robust fear memory so that it’s just a memory,” explained Conrad, who co-authored a paper on the idea published in the journal Neurobiology of Learning and Memory in 2015, titled “Chronic stress enhanced fear memories are associated with increased amygdala zif268 mRNA expression and are resistant to reconsolidation.”
The implications of being able to do that for sufferers of PTSD are enormous.
Conrad believes the ultimate goals of her research could be profound.
“I hope that we can have a better handle on how to manage stress. It’s complex; it underlies many psychological conditions from depression to anxiety to PTSD. By understanding more about the mechanisms that underlie it by using cognition as measureable outcome, we’re hoping that we can enable healthier lifestyles.”