In a panic attack, a person's heart rate shoots up, they may gasp for breath, sweat profusely and have a feeling of impending death.
Many people bounce back to normal functioning after stressful or dangerous situations have passed. Others may develop an acute stress disorder that goes away after a short period of time. But some go on to develop post-traumatic stress syndrome, which can appear after a time lag.
The stage is set for post-traumatic stress disorder after a stressful event causes a natural flood of glutamate, a neurotransmitter that excites the neurons. The excess glutamate dissipates after 30 minutes, but the neurons remain frenzied. The reason is the glutamate interacts with a second protein (Homer1a), which continues to stimulate the glutamate receptor, even when glutamate is gone.
For the study, Northwestern scientists first subjected mice to a one-hour immobilization, which is distressing to them but not painful. Next, the mice explored the inside of a box and, after they perceived it as safe, received a brief electric shock. Usually after a brief shock in the box, the animals develop normal fear conditioning. If they are returned to the box, they will freeze in fear about 50 percent of the time. However, after the second stressful experience, these mice froze 80 to 90 percent of the time.
The animals' exaggerated chronic fear response continued for at least one month and resembles post-traumatic stress disorder in humans, Radulovic said.
For the second part of the study, Natalie Tronson, a postdoctoral fellow in Radulovic's Dunbar Laboratory for Research on Memory and Fear, and Radulovic repeated the two stressful experiences with the mice but then injected them with MPEP and MTEP five hours after the immobilization. This time the mice did not develop the exaggerated fear response and froze for only 50 percent
|Contact: Marla Paul|