A single severe stressful event can cause delayed and long term psychological trauma. This is according to new research by Sumantra Chattarji of the National Center for Biological Sciences and the Institute for Stem Cell Biology and Regenerative Medicine in Bengaluru.
Chattarji’s team found that changes occurred in the amygdala (small node located in the central lobe of the brain associated with memory and emotional reaction) following a stressful event, according to UPI. This manner of activity is typical of post-traumatic stress disorder (PTSD). These changes are brought about by the formation of new neuronal connections called synapses, increasing electrical activity in the region.
“We showed that our study system is applicable to PTSD. This delayed effect after a single episode of stress was reminiscent of what happens in PTSD patients” Chattarji explained during a press release.
Chattarji’s study was conducted on rats. It found that, for ten days, no adverse effects were observed. However, following the ten day period, there was a notable increase in anxiety. The paper attributed this to delayed changes in the structure of the brain. These changes were found to occur both in the amygdala as well as the hippocampus.
One of the most notable findings of the study is the involvement of N-methyl-D-aspartate (NMDA) – receptors, an ion channel protein in nerve cells crucial for memory function within the brain. It is believed the neuronal plasticity required for the changes to take place following the stressful event are mediated by NMDA-receptors (NMDARs).
More experiments conducted in Chattarji’s investigations involved the use of NMDAR antagonist APV via targetted in vivo infusion to block NMDAR activity following the induced stress. It was found that inhibition of NMDARs stopped the formation of new synapses in the amygdala and reduced the increase in electrical activity in the area associated with stress induced change.
A commonly used NMDAR antagonist — memantine, used primarily in the treatment of Alzheimer’s disease has been tested in previous studies for treatment of PTSD, though this was primarily to address memory deficits. This study suggests that rapid treatment with the same medication, in the days following the event, would have far more beneficial effects.
The implications of this finding, and its close link in terms of mechanism to PTSD are that with the use of NMDAR antagonists following severe stressful events the occurrence of PTSD can effectively be prevented. Further studies are required along this line of thought, as it could bring about large scale improvements to mental health treatment, both in India and globally.
