The STRONG STAR Multidisciplinary PTSD Research Consortium
Abstract
The hypothesis addressed by this project is that early life exposure to stress or glucocorticoids produces a distinct neurochemical and behavioral phenotype characterized by life-long vulnerability to stressors that trigger PTSD. Last year we reported that the PTSD-like traumatic stress model we had adopted from the literature was deficient in several ways. Thus, over the past year, we have developed a new model of traumatic stress which has both construct and face validity as a PTSD-precipitating stressor. Moreover, we have developed an improved measure of fear conditioning and memory for the extinction of conditioned fear. We found that prenatal stress programs a sensitization to conditioned fear in the adult offspring, and a resistance to the extinction of conditioned fear. We also found that prenatal stress programs a unique neurochemical and hormonal phenotype that suggests possible mechanisms by which it can sensitize adult conditioned fear and impair extinction of conditioned fear. Specifically, we found that prenatal stress reduces TH expression in noradrenergic neurons in the LC region of the brainstem,increases basal corticosterone levels and reduces GR protein in prefrontal cortex. The chronically elevated corticosterone may explain the reduction in GR protein in the prefrontal cortex. Thus, we will now focus on noradrenergic corticosterone interactions in future studies of the role of early life stress in increased vulnerability and reduced resilience to stressors that precipitate PTSD.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 30, 2010
- Accession Number
- ADA544178
Entities
People
- Alan Frazer
- David Morilak
- Randy Strong
Organizations
- University of Texas at San Antonio