By: Adrian Smith
Stress causes changes to the hippocampus—the part of your brain responsible for memory and emotion, leading to anxiety and depression. However, researchers from Rockefeller University in New York have not only provided insight on these structural alterations in the brain, they believe they’ve found a way to prevent it moving forward.
Acetyl-I-carnitine, a molecule that is produced naturally both by humans and mice, is currently under testing as a treatment for depression. According to a survey done by the American Psychology Association, around 75 percent of Americans claim they’ve experienced a minimum of one symptom of stress this past month. Symptoms include anxiety, fatigue, depression and irritability.
As much as we know about how stress affects the hippocampus, few studies have investigated how stress affects the amygdala, which is the part of the brain involved in fear and anxiety. Researchers suggest acetyl-I-carnitine could have the ability to prevent harmful, stress-induced changes in the brain.
Carla Nasca and her research team at Rockefeller decided to look into this association by using mice to see how chronic stress affects their amygdala. They put mice in a small space periodically for 21 days in order to induce prolonged stress.
The researchers studied their behavior for any symptoms of anxiety or depression, such as avoiding social interaction. Researchers also analyzed the nerve cells of these mice in areas of the amygdala, such as the medial and basolateral regions. They found that neuronal branches in the basolateral region lengthened and became more complex in response to prolonged stress—an indication that they were flexible and able to adapt. However, they found that stress impairs nerve cell communication in the medial region, as nerves there shrink in response to stress.
Researchers repeated the same experiment, this time though, they used a different group of mice, and treated them with acetyl-I-carnitine 3 days before the end of their confinement. They found that the drug prevented neuronal brain shrinkage and that those mice treated with acetyl-I-carnitine were more sociable than the untreated mice of the original experiment. Their study included mice that are more prone to stress-induced anxiety and depression, in order to replicate humans who are more vulnerable to these conditions in response to factors of stress. Researchers hope this drug will be able to produce the same effect in human beings. Their next study will be to determine whether humans with depression have lower levels of acetyl-I-carnitine than those without.