Professor Page teaches in the Department of Biology and the Cell Biology and Biochemistry Program

Teaching Interests

I am lucky enough to teach what I love which includes both cellular and systemic physiology, more specifically, mammalian physiology. Currently my courses include:

  • Introduction to Molecules and Cells (BIO 205)
  • Neuroscience 100
  • Neurophysiology (BIO 324)
  • Independent Research (BIO 399)
  • Perspectives on Health and Healing (CAPSTONE)
  • Physiological Mechanisms (BIO 322)


Our studies are designed to investigate the effects of dexamethasone on gene expression of key hypothalamic-pituitary-adrenal axis negative- feedback regulation. Dexamethasone is a synthetic steroid analog of corticosterone, the major glucocorticoid secreted from the rat adrenal, and we found that prenatal exposure to this steroid results in HPA axis hyperactivity and increased levels of circulating CORT in the experimental animals. These studies are particularly pertinent for biomedical databases since dexamethasone is used clinically as a therapeutic to avert preterm delivery and to promote lung development in the fetus. It is important to investigate the long term effects of drugs that are used clinically, especially if the therapeutics are used during pregnancy. In addition, we are studying the effects of dexamethasone because it is a corticosterone analog and high levels of this hormone mimic the conditions of maternal stress. We are investigating how this physiological state in the mother would affect postnatal development in the offspring. We are especially interested in potential changes in gene expression that may underpin behavioral abnormalities.

We have already found that corticosteroid receptor expression in the brain changes in the DEX-exposed offspring. This change is particularly important since the ratio of corticosteroid receptor I (MR) and corticosteroid receptor II (GR) governs the “pulse” of hippocampal signaling to the hypothalamus. It has been hypothesized that a disturbance in this ratio may result in abnormal adrenal output of “stress” hormones such as cortisol (human) or corticosterone (rat) and that this disturbance may also alter serotonergic function since high levels of CORT affect serotonin function adversely. High circulating levels of CORT have been associated with reduced serotonergic transmission which may underpin affective disorders in humans such as anxiety and depression.


  • Creight Center Grant, awarded by Drexel University College of Medicine, 2007
  • Research Fellowship, awarded by the Population Council Center for Biomedical Research at Rockefeller University, 2000
  • Senior Research Fellowship Award, National Institute of Health, 1999
  • Research Grant, POWRE, National Science Foundation, 1998
  • Research Planning Grant, awarded by National Science Foundation, 1996


  • Presidential Award for Excellence in Teaching, Bucknell University
  • National Research Service Award, National Institute of Health

Selected Publications

*denotes Bucknell student author

Page K.C., Malik R.E.* and E.K. Anday. 2008. High fat intake during early development alters expression of leptin and insulin signaling components in hypothalamus of adult male rats. Under Review. American Journal of Physiology.

Shoener J.A.* and K.C. Page, 2006. Prenatal exposure to dexamethasone permanently alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity. American Journal of Physiology, 290:R1355-R1373.

Page K.C. 2004. “Quest for a Future Perfect,” eds. D. Rothenberg and W. Pryor, Writing the Future: Evolution and Progress, (Cambridge, MA; The MIT Press), 193-200.

Page K.C., Sottas C.E. and M.P. Hardy 2001. Prenatal exposure to dexamethasone alters Leydig Cell steroidogenic capacity in immature and adult rats. Journal of Andrology 22:973-980.

Wang G.M., Page K.C. and M.P. Hardy 2000. Leydig Cell Steroidogenesis. In What’s It All About: Androgens. American Society of Andrology. Boston, pp. 51-81.

Page K.C. 1999. Maternal exposure to dexamethasone markedly reduces testosterone synthesis in immature rat offspring. In: Cosmi E.V. ed. New Technologies in reproductive medicine, neonatology, and gynecology. Bologna, Italy: Monduzzi Editore, pp. 489-494

Page K.C., Heitzman D.A. *, and M.I. Chernin. 1996. Stimulation of c-jun and c-myb in Rat Sertoli cells following exposure to retinoids. Biochemical and Biophysical Research Communications, 222:595-600

Page K.C., Makris J.M. *, and M.I. Chernin. 1995. Effects of retinoids on the protooncogene, c-myb, in rat Sertoli cells. Recent Progress in Hormone Research. 50:465-469.

Page K.C., Mason P.B. *, Lindstrom L., Swan J.S., and S.E. Nyquist. 1992. Dolichol and N-linked oligosaccharide synthesis in the rat testis: Interaction between Sertoli and spermatogenic cells, evidence for paracrine effects. Biochemistry and Cell Biology,70:496-503.

Page K.C., Killian G.J., and S.E. Nyquist. 1990. Sertoli Cell Glycosylation Patterns as Affected by Culture Age and Extracellular Matrix. Biology of Reproduction, 43:659-664.


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