Sandra L. Petersen

Professor
sandyp@bio.umass.edu

Associate Dean of
the Graduate School and
Director of the Northeast Alliance for Graduate
Education and the Professoriate

Education
B.A., Rutgers University, 1978

M.A., Oregon State University, 1980

Ph.D., Oregon State University, 1984

Postdoctoral
1984-1988, University of Maryland School of Medicine

Research Interests

Three main projects in the lab:

I. Neural Mechanisms Regulating Ovulation in Mammals
Ovulation is a cyclic event that requires tightly regulated communication between the ovary and brain. As ovarian follicles approach maturity, they release increasing amounts of estrogen into the bloodstream. Fluctuating levels of estrogen increase the activity of specific neuronal systems in the brain which, in turn, signal the pituitary gland to release a surge of luteinizing hormone, the substance which induces ovulation. The neurohormone critical for signaling the pituitary gland to release luteinizing hormone, luteinizing hormone-releasing hormone (LHRH), is synthesized by fewer than two thousand neurons in the brain. Our research focuses on the intracellular and trans-synaptic signaling mechanisms by which estrogen regulates LHRH gene expression, biosysthesis and release.

II. Molecular Mechanisms by which Environmental Contaminants Disrupt the Neural Control of Ovulation
TCDD, a potent dioxin, has long been known to be a reproductive toxin in subhuman primates and rodents; however, little is known about reproductive outcomes in exposed human populations. We recently found that the aryl hydrocarbon receptor which binds dioxins, is expressed in the same brain regions that also have estrogen receptors. These regions are known to play a crucial role in the regulation of gonadotropin release. We are examining molecular mechanisms by which TCDD disrupts estrogen action in neurons of these regions.

III. Perinatal Effects of Estrogen and Dioxins on Sexual Differentiation of the Brain
Exposure to estrogen during development permanently alters the neural tissue that controls ovulation and other sexually dimorphic brain functions. Rapidly accumulating evidence suggests that exposure to dioxins (ubiquitous environmental contaminants) interferes with these estrogen action and/or exerts estrogen-independent effects on brain development by activating the arylhydrocarbon receptor (AhR). We recently demonstrated that estrogen receptor is found mostly in GABA neurons during development. Similarly, we found that the AhR is only in GABA neurons in brain regions that control reproductive function, thermoregulation, learning and memory. Importantly, each of these functions is permanently altered by a single, very low dose exposure to AhR ligands during development and also by developmental exposure to estrogen. We are currently examining mechanisms underlying estrogen-dependent sexual differentiation of the brain and determining how dioxin activation of the AhR interferes with these differentiation processes.

Recent Representative Publications

Ottem, N.E. and S.L. Petersen. 2004. Dual-phenotype GABA/glutamate neurons in adult preoptic area: Sexual dimorphism and function. Journal of Neuroscience 24(37): 8097-8105.

Hrabovszky, E., I. Kallo, A. Steinhauser, I. Merchenthaler, C.W. Coen, S.L. Petersen, Z. Liposits. 2004. Estrogen receptor-beta in oxytocin and vasopressin neurons of the rat and human hypothalamus: Immunocytochemical and in situ hybridization studies. J. Comp. Neurol. 473(3): 315-33.

Petersen, S.L., E.N. Ottem and C.D. Carpenter. 2003. Direct and indirect regulation of GnRH neurons by ovarian steroids. Biology of Reproduction 69: 1771-1778.

Curran-Rauhut, M. A. and S.L. Petersen. 2003. Oestradiol-induced temporal changes in tyrosine hydroxylase mRNA levels are not limited to subpopulation of A1 and A2 noradrenergic neurons with a high incidence of colocalization with oestrogen receptor-α or -ß mRNA. J. Neuroendocrinology 15(3): 296-303.

Flores, C.A., P. Shughrue, M. Lane, S.L. Petersen and S.S. Mokha. 2003. Sex-related differences in the distribution of ORL₂ receptor mRNA and colocalization with estrogen receptor mRNA in neurons of the spinal trigenimnal nucleus caudalis in the rat. Neuroscience 118: 769-778.

Ottem, E.N. and S.L. Petersen. 2002. Glutamatergic signaling through the NMDA receptor directly activates medial subpopulations of luteinizing hormone-releasing hormone (LHRH) neurons but does not appear to mediate effects of estradiol on LHRH gene expression. Endocrinology 143(12): 4837-4845.

Hays, L.E., C.D. Carpenter and S.L. Petersen. 2002. Evidence that GABAergic Neurons in the preoptic area of the rat brain are targets of 2,3,7,8-tetrachlorodibenzo-p-dioxin during development. Environ Health Perspect 110 (Suppl 3): 369-376.

Curran-Rauht, M.A. and S.L. Petersen. 2002. Regulation of glutamic acid decarboxylase 65 and 67 gene expression by ovarian steroids: Identification of two functionally distinct populations of GABA neurons in the preoptic area. J. Neuroendocrinology 14(4):310-7.

Curran-Rauhut, M.A. and Petersen, S.L. 2002. Distribution of progestin receptor (PR) mRNA in the brain stem of female rats. Gene Expression Patterns 1(3-4): 151-157.

Hrabovszky, E and S.L. Petersen. 2002. Increased concentrations of radioisotopically-labeled complementary ribonucleic acid (cRNA) probe, dextran sulfate and dithiothreitol in the hybridization buffer can improve results of in situ hybridization histochemistry. J Histochem. Cytochem. 50(10):1389-1400.

Hrabovszky, E., A. Stenihauser, K. Barabas, P.J. Shughrue, S.L. Petersen, I. Merchenthaler and Zs. liposits. 2001. RAPID COMMUNICATION: Estrogen receptor-ß immunoreactivity in luteinizing hormone neurons of the rat brain. Endocrinology 142(7): 3261-3264.

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