Research Proposal: Effects of Maternal Cortisol on Embryonic Neural Development

Abstract

Expectant mothers who experience periods of increased stress exhibit elevated expression of cortisol, a hormone that binds to glucocorticoid receptors in the hippocampus. Excessive exposure to cortisol can cause damage to glucocorticoid receptors and signal for the downregulation of glucocorticoid receptors – a process which handicaps future recognition of cortisol concentrations as well as the negative feedback loop responsible for regulating cortisol production. Placental transmission of maternal cortisol results in embryonic abnormalities pertaining to brain morphology, psychology, and various cardiovascular and metabolic functions. In this research proposal the expectant model organisms, rats, are given daily injections of 0 (saline), 0.5, or 1.0 mg of hydrocortisone acetate during days 15-19 of embryonic development to mimic periods of increased maternal stress and induce decreased glucocorticoid receptor density in the offspring. Following birthing, the pups are fixed and samples of hippocampal tissue are harvested for the application of a fluorescent antibody that facilitates visualization of glucocorticoid receptors and the subsequent quantification of optical density – a value that is predicted to be inversely proportional to the concentration of hydrocortisone acetate treatments. This essay was written in Dr. Osovitz class.