Psychological stress induces activation of a highly developed but conserved physiological system called the hypothalamic‐pituitary‐adrenal (HPA) axis, which is ultimately regulated by glucocorticoid negative feedback. The HPA axis is active in both a tonic way, manifested as a diurnal hormonal secretion pattern, and in an acute way, as a phasic, stress‐responsive surge in hormones. In addition to eliciting hormonal responses, stress elicits within the HPA system various genomic alterations, like regulation of expression of the corticotropin‐releasing hormone (crh) gene in the paraventricular nucleus of the hypothalamus. Moreover, glucocorticoid negative feedback also entails regulation of crh gene expression. However, the specific mechanisms by which stress and glucocorticoids regulate crh gene expression are largely unknown. A proposed coactivator for the crh gene transcription factor CREB is a class of proteins known as transducer of regulated CREB activity (TORC) proteins, especially the hypothalamic isoform TORC2, which have been shown in vitro to be highly responsive to cellular stimulation. However, studies within live animals regarding TORC proteins are limited, and the goal of this project was to investigate TORC2’s responsiveness to both acute psychological stress and tonic secretion of glucocorticoids in rats. Although preliminary evidence was convincing, there was no effect for either acute stress (15 minutes restraint‐stress) or tonic glucocorticoid secretion on TORC2 activity, while hormonal data indicated typical HPA axis responses to these manipulations.
Highland, Julie, "TORC2 Reactivity to Acute Psychological Stress and Tonic Glucocorticoid Secretion" (2011). Undergraduate Honors Theses. 633.