Wednesday, December 11, 2019

Neurological and Biological Factors of PTSD





Dr. Michael Fanselow, a successful researcher and professor at the University of California, Los Angeles began his lecture by mentioning the effects and implications of PTSD. He reported that 10-20 percent of people go on to experience PTSD symptoms due to suffering from a traumatic event. In America, more than 8 million people ages 18 and above suffer from symptoms of PTSD. In regards to Dr. Fanselow’s research, he goes on to talk about what happens in a traumatic experience that could cause symptoms of PTSD in individuals. PTSD can also lead to depression and changes in in long term mood and behavior. In Dr. Fanselow’s articles “Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress” he and other researchers explore the effects of corticosterone (CORT), in stress enhanced fear learning (SEFL) within rodents. Researchers then discovered that the SEFL is allowed by CORT to make changes to the basolateral amygdala (BLA) through increasing the expression of excitatory receptor GluA1 AMPA. Researchers used metyrapone, a synthesis blocker to test the necessity of CORT. The results implied that CORT changes at moments of stress are paramount for SEFL. The research also solidifies the idea that preventing the up-regulation of GLuA1 helps prevent SELF from developing a stressor, thus helping mitigate the effects of PTSD.
On the other hand, PTSD is affected through many factors other than just manipulating receptors within the brain. PTSD is also shown to be affected through experiments on the immune system. In the news article titled “Immunization Could Halt Post-Traumatic Stress” the author compiles research information from Chistopher Lowry, a neuroscientist at the university of Colorado boulder, in which Lowry discusses results from experiments testing the link between fear and immune response.  Lowry’s team mentions that soldiers who have high levels of inflammatory protein CRP in their blood are more likely to develop PTSD. In order to test the hypothesis that tweaking the immune system directly affects fear and anxiety. Scientists injected mice with common bacteria M. vaccae and saw that mice that were injected were more proactive in dealing with aggressors. To test the loss of fear and anxiety, rats were conditioned to fear a sound associated with an electric shock to the foot. The scientists then extinguished this fear in immunized rats and control group rats. The results showed that immunized rodents lost symptoms of fear and anxiety much quicker than the control group. These results could mean that clinical treatments could be effective in patients who suffer from PTSD symptoms, as this form of immunomodulation, coupled with therapy can speed up the process of combatting PTSD.
All in all, both these research articles in conjunction show that PTSD is a very complex disorder, and there are many factors which hold influence over how it affects an individual. Treatments for symptoms of PTSD are not limited to just genetics and receptors in the brain, but also include somatic responses as well as alterations in the immune system. By putting together the neural and biological factors behind PTSD, researchers can further their studies and effectiveness in treatments regarding fear and anxiety. Through Dr. Fanselows research we can gain further insight into the mechanisms of PTSD, and apply what we learned from Christopher Lowry’s work to help discover an effective treatment option for those who suffer from PTSD. I hope to see more results from these studies as a handful of people in the states suffer from this disorder.
Works Cited
Reardon, S. (2015, June 15). Immunization Could Halt Post-Traumatic Stress. Retrieved from https://www.scientificamerican.com/article/immunization-could-halt-post-traumatic-stress/.

Perusini, J. N., Meyer, E. M., Long, V. A., Rau, V., Nocera, N., Avershal, J., … Fanselow, M. S. (2015). Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress. Neuropsychopharmacology41(1), 45–57. doi: 10.1038/npp.2015.224

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