Phillip Zoladz, an Associate Professor of Psychology at Ohio Northern University, received his Ph.D. in behavioral neuroscience from the University of South Florida in 2008. Dr. Zoladz’s expertise is in the areas of stress, emotional memory formation, and post-traumatic stress disorder. Dr. Zoladz oversees two research laboratories at Ohio Northern University, one involving rodent research and one involving human research. The research in both laboratories is focused on the neurobehavioral consequences of psychological stress and has received funding from the National Institutes of Health.
Susceptibility for PTSD
Individuals who are exposed to trauma are at risk for developing post-traumatic stress disorder,
or PTSD. One of the cardinal symptoms of PTSD is a powerful, often intrusive, memory of the
traumatic event. This memory can prompt the onset of flashbacks and motivate PTSD patients
to avoid stimuli that remind them of their trauma. Although the traumatic memory is often
considered an enhanced memory that is easily accessible, it can actually be fragmented and
difficult to consciously recall.
Only a subset of traumatized individuals experience prolonged symptoms that warrant a
diagnosis of PTSD. Thus, there is interest in identifying factors that make select individuals
more susceptible to developing PTSD-like phenotypes following trauma exposure. We have
been using a basic science model in healthy individuals to examine factors that influence
emotional memory formation, which could provide insight into who is more likely to develop
traumatic memories and, potentially, PTSD.
In our model, participants are exposed to a brief, 3-min stressor, after which they are given a
learning task. We previously found that stressing participants immediately or 30 min before
learning enhanced or impaired long-term memory, respectively. Thus, we predicted that some
individuals may be more susceptible to these effects.
Recent work testing this hypothesis revealed that our previously-observed stress-induced
alterations of memory were greatly amplified in individuals who retained variants of genes
coding for stress response proteins, such as receptors for cortisol and noradrenaline. We also
found that females are relatively resistant to stress-induced impairments of memory and may be
more susceptible to stress-induced enhancements of memory. We are currently following up
this work by examining how these genetic variants and sex influence the extinction of fear
memories, a process that is central to exposure therapy but often impaired in PTSD patients.