A team of researchers from India have discovered how a single incident of trauma causes a delayed onset of debilitating psychological stress, which is experienced for a long period of time.
Amygdala And Post-Traumatic Stress Disorder
The researchers also unraveled the psychological and molecular events associated with the process. It is noted in the study that the stressful event increases the electrical activity of a specific region of the brain called as amygdala.
The onset of the symptoms usually begin in about 10 days after the incident and a compound known as N-Methyl-D-Aspartate Receptor (NMDA-R) plays a key role in the process. NMDA-R, which is a protein in the ion-channel of the neurons, is responsible for functions such as memory.
Amygdala, which is found deep inside the temporal lobe, is made of small group of neurons. This part of brain is known to control functions such as decision making, memory, and emotions. Post-Traumatic Stress Disorder (PTSD), a psychiatric condition experienced by a person after a traumatic incident develops due to alternations in amygdala.
Mechanism Involved In Post-Traumatic Stress
Sumantra Chattarji, the lead author of the study at National Centre for Biological Sciences (NCBS), said that the current study is applicable for PTSD since the activity of amygdala is intense in patients suffering from it. However, the mechanism involved in the process is not found by far, added Chattarji.
After experiencing a trauma, minute structures in the neurons of amygdala region of a person's brain undergo major alternations. As a result, new nerve connections known as synapses are formed in this area of the brain.
Farhana Yasmin, who is also a part of the study, said that studies conducted by far focused on stress experienced on repetitive basis and single stressful episode that inflict changes immediately, for instance a day or two. However, the current study deals with a single episode of trauma that causes changes after a week or so, added Yasmin.
Role Of NMDA-R In Post-Traumatic Stress
The researchers, who identified that NMDA-R is the key component in causing the changes, tested it on the ailment. It was found that when NMDA-R was blocked it not only put an end to the formation of synapses but also controlled the electrical activity taking place in the synapses.
"So we have for the first time, a molecular mechanism that shows what is required for the culmination of events ten days after a single stress," said Chattarji in a press release.
Chattarji also added that in the current study, the protein NMDA-R was blocked during stress; however, it is necessary to check if blocking the compound immediately after the stressful incident would help manage the problem. In that case, how long after the incident the protein can be blocked for effective intervention needs to be studied.
The study is published in the journal Physiological Reports.
