At 5:04 p.m. on October 17, 1989, two decades after he served as a combat soldier in Vietnam, Lance Johnson felt the tremors of San Francisco’s Loma Prieta Earthquake from his apartment in Marin County. He took his cup of coffee to the couch, switched on the news and saw a live feed of the fire and destruction happening 40 miles south. Suddenly, he was hit with some of the common symptoms of post-traumatic stress disorder (PTSD). As he recalls: Someone tripped a switch in my head, and instantly, I was back in Vietnam. In my mind, the concept of time suddenly meant nothing, and I traveled a wormhole in space from San Francisco to twenty years earlier in Southeast Asia. Panic. I didn’t know what to do.*
You don’t have to be a combat vet to know that your response to stress—whether a loud noise, dying relative or looming deadline—changes over time. After the first exposure, we are somehow primed for the next, even weeks or years later. And when something in that process goes wrong, the consequences can be tragic.
Neuroscientists don’t understand much about how the brain encodes such a versatile stress response. It’s part of a complicated mess of hormonal, chemical and electrical signals in a brain system called the hypothalamic-pituitary-adrenal (HPA) axis. A new rat study has made the picture slightly less muddled, opening the door a tiny bit to new treatments for PTSD and other types of chronic stress.
Now, brace yourself, I have to tell you first about how the researchers stressed out the rats. They did it in two ways—one social, one not—and neither is pleasant to think about. In one test, they placed an open vial on top of the rat’s cage that contained the frightening scent of fox feces. In the other, they immobilized the rat for 30 minutes in a ‘plexiglass restrainer’. After each stress session, they killed the rats, sliced up their brains and recorded the electrical activity of neurons in the HPA.
Both types of stress produced dramatic changes in cells of one particular region—the paraventricular nucleus—that lasted for several days. These cells were primed: after stimulation, they showed stronger chemical responses at the synapse, the junction between neurons, than did control cells.
In an elegant series of experiments, the scientists uncovered many steps of the molecular cascade that causes this priming. This is a blog, so I’ll spare you the details, but knowing each and every step of the process is hugely important for developing potential stress therapies. For example, the researchers found that they could prevent the cellular priming if, before the stress session, they injected the rats with a drug that blocks a certain kind of receptor. The implication is that there’s hope—way, way down the road—for un-priming the overly sensitive stress responses of people like Lance Johnson.
*I found Lance’s story on this website, which has several gripping accounts of Vietnam soldiers who experienced PTSD.
This post was originally published on The Last Word on Nothing