Vadim E. Tseilikman, Ph.D., D.Sc.
Professor of Pathophysiology & Biochemistry
Director, School of Higher Medical Biology
South Ural Medical University, Russia
“Neuroendocrine and biochemical mechanisms of post-traumatic stress disorder”
Post-traumatic stress disorder (PTSD) is a delayed consequence of severe psychic trauma. Glucocorticoid levels are lower in PTSD patients. In our rat model of PTSD, low corticosterone levels were associated with morphological damage to the adrenal fasciculate zone. Also, we found that the PTSD-induced glucocorticoid degradation was activated in the adrenal glands. In addition, decreased activity of monoaminoxidase A (MAO-A) correlated with increased norepinephrine in the brain cortex, hippocampus, cerebellum, and brain stem. Considering that glucocorticoids participate in up-regulation of MAO-A gene expression, we propose the following mechanism of PTSD development: decreased glucocorticoid production in adrenal glands → decreased corticosterone concentrations → decreased MAO-A activity in the brain → increased brain norepinephrine → increased anxiety intensity → stress-related behavioral disorders.
Friday, November 2, 2018, 11:00AM-12:00PM, LIB-110
University of North Texas Health Science Center
Fort Worth, Texas