Brent Myers, Ph.D.
Assistant Professor, Department of Biomedical Sciences
Colorado State University
“Cortical circuitry integrating the cardiovascular and neuroendocrine consequences of chronic stress”
Stress, defined as a real or perceived threat to homeostasis or well-being, has a considerable role in the pathogenesis of mood and anxiety disorders. Moreover, prolonged stress and mood disorders are significant risk factors for numerous cardiometabolic conditions that further burden health-related quality of life. The neurobiological mechanisms of stress-related health detriments remain elusive; however, we have identified a specific population of chronic stress-activated glutamate neurons in infralimbic cortex that integrate behavioral and physiological responses to stress. Large-scale quantitative circuit mapping in rats identified a network of projections from these cells to numerous behavioral and homeostatic regulatory regions. Furthermore, knockdown of vesicular glutamate transporter 1 (vGluT1) in infralimbic cortex was employed to reduce presynaptic vesicular glutamate packaging and excitatory outflow from infralimbic cortex in rats undergoing chronic variable stress. vGluT1 knockdown and chronic stress interacted to increase basal and stress-induced corticosteroid secretion, enhance heart rate reactivity to stress, elevate chronic blood pressure, and induce vascular endothelial dysfunction. Additionally, optogenetic activation of infralimbic glutamate neurons induced place preference and increased social motivation. This was coupled with reduced autonomic and endocrine stress reactivity. Collectively, these studies highlight infralimbic cortical neurons as a critical component of the neural networks mediating stress chronicity and the adaptive integration of behavioral strategy with physiological status.
Friday, November 9, 2018, 11:00AM-12:00PM, LIB-110
University of North Texas Health Science Center
Fort Worth, Texas