Post-traumatic stress disorder can be a debilitating condition. It’s estimated that it affects nearly one in 10 Canadian veterans who served in Afghanistan. Now, there’s promising research that could lead to the treatment of the disorder.
Following a particularly traumatic event — one where there is the serious threat of death or a circumstance that was overwhelming — we often exhibit physical symptoms immediately. But the effects in our brains actually take some time to form. That’s why symptoms of PTSD — reliving an event, nightmares, anxiety — don’t show up until some time later.
Research has shown that, after such an event, the hippocampus — which is important in dealing with emotions and memory — shrinks, while our amygdala — also important to memory and emotions — becomes hyperactive.
In earlier research, Sumantra Chattarji from the National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), in Bangalore, India, discovered that traumatic events cause new nerve connections to form in the amygdala, which also causes hyperactivity. This plays a crucial role in people dealing with post-traumatic stress disorder.
Chattarji has been studying changes in the brain after traumatic events for more than a decade. In an earlier study, he concluded that a single stress event had no immediate event on the amygdala of rats.
However, 10 days later, the rats exhibited increased anxiety. There were even changes to the brain, and, in particular the amygdala. So Chattarji set out to see if there was a way to prevent these changes.
The new research focused on a particular cell receptor in the brain, called N-Methyl-D-Aspartate Receptor (NMDA-R), which is crucial in forming memories.
“Clearly in PTSD, it’s the memory of the trauma that keeps coming back, and that becomes the debilitating symptom: you want to forget, but you can’t forget,” Chattarji told CBC News.
So, in the experiment, the researchers blocked NMDA-R during the traumatic episode. The results were encouraging: first, no new nerve connections formed, and secondly, there was no hyperactivity in the amygdala 10 days later.
Timing is key
“For the first time we’ve identified a potential therapeutic target which can be acted upon to block the delayed effects of stress,” Chattarji said.
But the key is timing.
“We cannot wake up every morning and, in anticipation of stress, just take a pill,” Chattarji said.
Instead, the next step in the research is determining how soon after the episode — or even how long after — the receptor can be blocked and produce similar results. Ascertaining this would lead to potentially therapies for those living with PTSD, Chattarji said.
“What we’re trying to do is to see how long after the end of stress can we still make this intervention and block the effects,” he said.
Initial results from followup research suggest they can block the receptor an hour and even up to a day after the stress-induced event.
Now, a generic blocking of the NMDA-R would have implications on forming new memories in general.
“Since NMDA receptors are needed for forming memories — a generic blocking will indeed be a problem. That is why we cannot simply block this receptor in anticipation of a traumatic experience, because that may impair the formation of other memories as well,” Chattraji said.
“However, at the time of the trauma, having the blocker on board would help prevent that experience from becoming of the source of subsequent emotional symptoms in the amygdala.
“So, it is a fine balance.”
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