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ou park your car. After spending the day at work, you remember precisely that you left it on the second floor, facing toward the exit. As you use your remote key to pop the trunk so you can put your bag away, the car blows up, launching you into the concrete wall behind you. Battered and bleeding, you wonder whether you’ll live, and who is out to get you. The sensations of the scene—the obliterated car, the searing pain—trigger the amygdala, the brain’s seat of emotions, where the shock of the event will continue to resound. The hippocampus will record all those precise details. For the next 48 hours, your brain will be flooded with protein molecules called AMPA receptors (AMPARs) that will make the event unforgettable. The persistence of memory will become your enemy. Surrealistic shards of the event will live on in your fitful sleep and during unrelenting anti-reveries. What is going on? The amygdala, an almond-shaped region of the brain that sits just in front of the hippocampus, reacts to trauma with a fear response that charges the neural circuitry, while other parts of the brain work to inhibit the fear. The problem in people suffering from post-traumatic stress—about 8 million in the United States—is that the
amygdala and the lingering memory stored in the hippocampus continue to reign. “Often, therapists can modify people’s responses to traumatic events through behavioral therapy, but relapse is very common,” says Richard Huganir, professor of neuroscience at the School of Medicine, adding that the memory of the event is not completely “erased” during such therapy. “The problem is that the fear response can be summoned up long after the fear conditions have been removed.” Last year, Huganir and postdoctoral fellow Roger Clem published results of research on experimental mice, in which the duo investigated the role AMPARs play in keeping our waking nightmares alive. They found that the receptors increase during the so-called fear-conditioning period, which peaks at about 24 hours after trauma and dissipates at around the 48-hour mark. AMPARs, unlike most substances in the brain, are unstable and can conceivably be removed from cells. It’s possible that a drug could be developed to block and sweep away receptors that make fear indelible in the mind. Huganir hopes that his and other Johns Hopkins scientists’ findings on the functions of brain chemicals will lead to treatments, likely many years down the road, that
Exploring the Link between Art and Memory
36 36 JJohns ohns H Hopkins opkins M Magazine agazine • •W Winter inter 2011 2011
Courtesy of Prof. Barbara Landau
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our years ago, Lonni Sue Johnson’s life story was as rich and vivid as her work. An artist of precisely detailed, often witty drawings—several had graced the cover of the New Yorker and the business page of the New York Times—Johnson also regularly bowed her viola and piloted planes. Suddenly, that story all but disappeared. One snowy day, a neighbor stopped by Johnson’s upstate New York organic dairy farm and found the usually effusive and alert Lonni Sue doing little more than staring at her computer mouse. Something was clearly wrong. After being driven to a hospital, an MRI showed that the center of her brain had been ravaged. The cause, viral encephalitis, came with a high fever that almost killed her. Although her life was ultimately spared, her hippocampus had been wiped out, along with the memories that are formed and stored there. With the help of her family, she began to rebuild her life, albeit tenuously—her grasp of events remained slippery. Johnson was totally disabled. She had to learn to walk and talk again. Much of the cultural and intellectual knowledge she once held had been erased from her
memory banks. Even Van Gogh’s Starry Night became a stranger to her. And yet, the personality of her art—the gracefully curving lines, the playful sense of humor—began to announce itself anew as she recovered. In all that lay a source of fascination for scientists. In 2009, Barbara Landau, a former high school classmate of Johnson’s in Princeton, New Jersey, heard about her case. Landau, a professor of cognitive science at the Krieger School, spoke with Johnson’s family about having Lonni Sue take part in research that would examine the effects of
viral encephalitis on brain function and creativity, and the family enthusiastically agreed. Landau and other Krieger School scientists have found that Johnson, now 61, suffers from amnesia of events both before and after her bout with encephalitis, and that she is unable to form new memories. And yet, much of her artistic skills remained intact, though she needed to be retrained in the use of a pencil and still requires encouragement to keep developing her innate skills. “One hypothesis you can make from her case is that you don’t need