What if there were a drug that could prevent the development of PTSD (Posttraumatic Stress Disorder) in those at risk? A study published today in the Proceedings of the National Academy of Sciences offers new insight into how the brain processes traumatic memories. Researchers say these discoveries could lead to just such a treatment.
Scientists at McLean Hospital near Boston found that the surge of noradrenaline, a neurotransmitter released during stressful events, can cause the brain to consolidate traumatic memories in a way that can result in the vivid flashbacks that plague victims of PTSD. This information may be the key to developing a drug that interrupts that process and stops the disorder from taking hold in the minds of those at risk--like recent rape victims or soldiers who've experienced devastating battlefield events.
NEWSWEEK's Temma Ehrenfeld spoke to Vadim Bolshakov, director of the Cellular Neurobiology Laboratory at McLean Hospital, about the research and how his team's work with rats could help prevent PTSD. Excerpts:
NEWSWEEK: The public became more aware of PTSD when we learned that Vietnam vets were having debilitating flashbacks and nightmares. Now soldiers home from Iraq are suffering too. How does PTSD develop-can any kind of trauma cause it?
Vadim Bolshakov: Any psychological trauma could lead to PTSD. In our lab, we model trauma by giving a rat a mild electric shock on the foot after a loud sound. The next time it hears the sound, it associates the sound with the shock and shows what we call a "fear response." It freezes or startles and we can measure a raised heartbeat. In a human being, a sound or smell can bring the painful memories back. The human being doesn't necessarily freeze or startle, but experiences other symptoms that are part of the fear response.
You found that the release of noradrenaline leads to the formation of permanent memories linked to the fear response. How is noradrenaline different from adrenalin, the chemical that makes us feel excited before a race or speech?
Noradrenaline, which is released in the brain, has many complex roles, but one of them is to help us acquire memories with emotional significance. It's why you are likely to remember what you were doing on September 11, 2001. Adrenalin is a different chemical released by the adrenal glands, but often at the same times, when we are under stress.
There's a lot of excitement about the idea that it might be possible to give people a drug in emergency rooms, soon after rapes and traffic accidents, for example, that would prevent the long-term fear association from forming.
Our study provides basic science support for that idea. Our data shows that manipulation of the noradrenaline system in the brain could be used to treat PTSD and it should be as soon as possible after the trauma. The medication now being used experimentally in emergency rooms is the beta adenoreceptor blocker propranolol, a hypertension drug. Prazosin is another interesting possibility. These drugs block the receptors that are activated by noradrenaline.
Could these drugs work later, with distant trauma?
It's possible. We also know that each PTSD reaction is a recall of the painful memory. Drugs could be taken after a retriggering of the PTSD, when the memory is moving from short-term to long-term again. Some of the current medications for PTSD are antidepressants, which just remove anxiety secondary to the trigger of PTSD.
Why don't we don't have flashbacks to positive memories like our first kiss when we're hyped up?
The release in noradrenaline affects the amygdala, which is mostly activated by bad memories. Positive memories are distributed within different brain regions.
You did your research looking at slices of a rat's brain under a microscope. Wouldn't a human brain be very different?
The neural mechanisms are extremely similar, and you could see the same brain structure. You could locate the amygdala, the part of the brain associated with negative emotions. In our earlier study we showed that fear conditioning led rats to have more electrical currents coming to the amygdala. Looking at slices of the brain, we recorded the tiny electrical currents flowing between the neurons. This time, we injected the slices of brain with noradrenaline and measured the changes in the electrical currents. We found that by adding the noradrenaline, it takes less stimulus to create "LTP" or long term potentiation, when the increase in currents [in the amygdala] becomes long-term [which is associated with PTSD].
What's the next step?
We want to inject the animals with blockers for noradrenalin receptors before fear-conditioning to see if that would suppress the creation of long-term memories. This would help us see whether drugs that block noradrenalin receptors in the amygdala could be helpful.