Meeting Abstract
P1.69 Thursday, Jan. 3 Glucocorticoids Suppress Stress-Induced Activation of Extracellular Signal-Regulated Kinase in the Paraventricular Nucleus of the Hypothalamus LEID, L.*; JARVIS, E.; SPENCER, R.l.; Medgar Evers College; Univ. of Colorado, Boulder; Univ. of Colorado, Boulder catapane@mec.cuny.edu
Mitogen- activated protein kinases (MAPKs) are involved in the intracellular pathways that respond to various extracellular signals. Extracellular signal regulated kinase (ERK) is a member of the MAPKs family. During a period of stress, cellular ERK becomes activated in the Paraventricular nucleus (PVN) of the Hypothalamus. The hypothalamus is the initiation site for the HPA axis in response to stress and direct negative feedback by glucocorticoids. Glucocorticoids are hormones that modulate the stress reactions. It is thought that the interruption of this pathway may inhibit these signal transduction response mechanisms that in turn may alter the secretion of hormones in the body during stress. This experiment focused on the effect that glucocorticoid negative feedback has on the activation of ERK. In this experiment we applied a 2 x 2 factorial design using Sprague Dawley rats (N=16). Half of the rats were adrenalectomized, ADX, (n=8) and SHAM surgery was performed on the remainder (n=8). Half of both groups were either subjected to no stress or 15 min restraint stress. Immunohistochemistry was used to determine the activation of ERK in the PVN. Acute restraint stress produced detectable amounts of activated ERK. ADX stressed rats showed a significantly increased amount of activated ERK than SHAM stress rats. ADX and SHAM no stress rats showed no big differences in the activation of ERK. These results suggest that it is feasible to inhibit the activation of ERK with glucocorticoid pretreatment. This project was supported by the SMART Program of the University of Colorado, Boulder. Lucy Leid is a participant in the CSTEP and NSF-STEP programs of Medgar Evers College which are funded by grants 0516041071of NYSDOE and 0622197 of the DUE Program of NSF.
