It is well-known that the symptoms of post-traumatic stress disorder (PTSD) are precipitated by traumatic events or highly stressful experiences, including events that happened early in life. New research from a team led by a NARSAD Distinguished Investigator Grantee adds a surprising new dimension to this. They have found that it may not be necessary for one to explicitly remember a stressful or traumatic event for it to cause PTSD.
Michael S. Fanselow, Ph.D., of the University of California, Los Angeles (UCLA), a 2011 NARSAD Distinguished Investigator Grantee, and colleagues reported August 15th in Biological Psychiatry that an adult suffering PTSD symptoms may have no recollection of any childhood trauma whatsoever if the trauma occurred during a period early in life before the brain is wired to recall memories.
The new finding does not pertain to the often debilitating PTSD symptom of flashbacks brought on by cues in the environment linked to an original trauma. To have a flashback, one has to have a memory of the event, which often includes such details as odors, sounds, time of day and place.
Dr. Fanselow’s team conducted experiments in very young rats—animals 19 days old, at a stage of development just before the rat brain becomes able to form “explicit memories,” or those that can be voluntarily recalled and described. These juveniles were exposed to a single session of unpredictable stress (foot shocks). Then, after maturing to adulthood, they tested the animals for their memory of the event and also measured their fear response.
The researchers treated a part of the animals’ cages with a pungent odor during the stressful experience to serve as a later cue for the event. The rats did not show evidence of remembering the stress or the environment in which it occurred. “But they did show a persistent increase in anxiety-related behavior and increased learning of new fear situations,” said team member Andrew Poulos, Ph.D., of UCLA. One of the anxieties noted was a mild aversion to the odor associated with their stress. In people with PTSD and vivid fear memories, such sensory cues can be quite severe.
In related experiments, Dr. Fanselow’s team noted other irregularities in the adult rats that had experienced early-life stress. The daily rhythms of the stress hormone corticosterone in their systems was altered––they had more “docking ports,” or cellular receptors, for this hormone in neurons of the amygdala, a known fear center. In future experiments, the team will try to determine if it is indeed the greater availability of such receptors—and/or the shifts in hormone levels during the day—that cause the increased fear and anxiety.
"These data highlight the importance of the many ways in which the brain processes traumatic experiences,” commented Foundation Scientific Council member John H. Krystal, M.D., Editor of Biological Psychiatry. “Psychotherapy tends to focus heavily on the articulation of trauma memories. However, the current study highlights that these explicit memories may not represent all brain processes that drive distress and disability. In other words, there may be a mismatch between what people think and how they feel about their traumatic experiences. Thus, there may be a role in treatment for measuring other dimensions of response, such as physiologic arousal, through which some of these other forms of learning are expressed."