Liberzon/Chen Lab (Bryan)
Stress Neurobiology lab
Post-traumatic stress disorder (PTSD) is a chronic, debilitating disorder that can emerge following trauma. It is a very common psychiatric disorder, with a lifetime prevalence in the US at 6.8% (16-17% in veterans). PTSD is characterized by a wide range of symptoms including hyperarousal, avoidance, intrusive memories and abnormalities in fear responses. We seek to understand the factors that contribute to PTSD etiology and the aspects altered by the experience of trauma and development of the disorder.
Areas of Focus
Animal models of PTSD, Single Prolonged Stress (SPS) – Led by Dr. Liberzon
Dr. Liberzon created the SPS model of PTSD decades ago and it is widely adopted and the most commonly used PTSD animal model with > 400 publications. The resulting phenotype from SPS mimics closely the deficits and neurobiological changes seen in PTSD patients, namely, increased startle, deficit in extinction recall and an abnormal hypothalamic-pituitary-adrenal axis function. This model has been, thus, useful in the study of molecular, neuroanatomical and functional alterations associated with PTSD phenotype. Currently, this model is used in the Liberzon laboratory to: 1) determine if SPS disrupts extinction retention by altering extinction retrieval/consolidation, fear reconsolidation, and/or contextual modulation of extinction/retrieval, 2) demonstrate that the SPS enhancement in brain GR and β-AR expression alter glutamatergic and GABAergic function in neural circuits that mediate SPS-induced deficit in extinction retention, 3) demonstrate that pharmacological treatments that act at GR and β-AR, or normalize excitatory neural processing, prevent SPS-induced extinction retention deficits, and 4) examine candidate vulnerability/resilience factors that interact with SPS exposure and demonstrate their effects on extinction retention and SPS-induced GR (and β-AR) upregulation and 5) provide novel insight into the role of hippocampal-prefrontal projections in stress-induced impairments in extinction retrieval via fiber photometry, optogenetics, chemogenetics, and neuropixel based electrophysiology.
Sex differences in stress and trauma – Led by Dr. Chen
Women are twice as likely as men to develop PTSD after trauma, even after accounting for the type of trauma. This suggests that a trait inherent in being female might modulate the risk for PTSD in women and that, perhaps, treatment should be sex dependent. Preliminary data demonstrates that, in freely cycling female rats, exposure to trauma during proestrus period, when female gonadal hormones peak, might increase the risk for later developing PTSD-like symptomatology. Current work investigates which gonadal hormone(s) are responsible for this increased risk, their mode of action, and potential early interventions.
PTSD and Risk for Heart Disease – Led by Dr. Chen
PTSD has been associated with a 55% increase in risk for incident coronary heart disease (CHD) or cardiac-specific mortality, regardless of demographic or clinical/psychosocial factors. It is known today that the diagnosis in PTSD often precedes that of heart disease, yet, it is not known what factors present in PTSD affect heart disease etiology. Currently, we investigate the epigenetic and metabolic changes that occur in brain, heart and blood following trauma exposure and emergence of PTSD-like symptomatology in animal models. Understanding the connection between these two diagnoses may aid in determining early detection tools as well as develop more comprehensive treatment strategies for these patients.
Lab Team Members
TAMU Collaborators
Outside Collaborators
Contact Us
If you are interested in more information, please, contact Dr. Chen at chiehchen@tamu.edu.