It probably goes without saying that post-traumatic stress disorder (PTSD) and fear go hand-in-hand. But new research is uncovering ways in which the brain’s fear response may play a crucial role in the development of PTSD, as well as suggesting possible causes of abnormal changes in the brain’s fear circuitry.
The Mechanism of Fear
Researchers at Vanderbilt University Medical Center have examined the way that rats respond to threats, both real and imagined. In the process, they may have discovered the mechanism of the fear response in the brains of PTSD sufferers. The secret may lie in the way that different parts of the brain communicate with one another.
Neurologists know that a part of the brain called the cerebral cortex is responsible for determining when a threat is present. The cerebral cortex then passes that information on to a relatively primitive part of the brain called the amygdala, which then triggers the familiar “flee-or-freeze” fear response.
The Vanderbilt researchers found that, in the rats they studied, communication between the cerebral cortex and the amygdala went through two separate and distinct channels. One channel seemed to be responsible for turning on the rats’ “freeze” response, and the other channel was responsible for turning off the response when the threat was gone.
The researchers theorize that PTSD might arise when the “off-switch” channel does not function properly, causing the sufferer to “freeze” in the presence of a fear trigger and then have trouble realizing when the threat is no longer present.
“It’s like they’re stuck on the freezing channel and can’t flip back to the normal behavior channel,” says Sachin Patel, MD, PhD, one of the study’s authors. “That’s a theory (but) it might be related to some sort of deficit in this synaptic flexibility mechanism we’ve discovered.”
Patel thinks it’s possible that the two channels might be chemically different, which would open the door to potential drugs that could put the fear response back in the proper balance.
PTSD and Brain Injuries
Another study, this one conducted by researchers at UCLA, is shedding some light on one possible cause of changes in the amygdala that could lead to PTSD. The study looked at the fear response in rats that had sustained a concussion-like brain injury. When frightened by an electric shock, the injured rats tended to freeze for a longer period of time compared to uninjured rats. The injured rats also tended to freeze when they heard a noise associated with the shock, even when there was no actual shock.
When the researchers examined the injured rats’ brain activity, they found that the rats’ amygdalas were much more active when they heard the noise than were the amygdalas of the uninjured rats. The injured rats’ brains also seemed to use a primitive area called the thalamus to process the noise, rather than the relatively sophisticated auditory cortex, which normally processes sounds.
“It’s almost as if the white noise acted like the shock,” says Michael Fanselow, PhD, the study’s senior author. “The noise itself became scary to them, even though it wasn’t much noise. They treated it almost like a shock.”
As is the case with the Vanderbilt study, the hope is that a more thorough understanding of the chemical relationship between the amygdala’s activity and PTSD could lead to treatments for the disorder, either through new therapies or future medications.