Sally J. Pyle

(701) 777-3699

sally_pyle@und.nodak.edu

Associate Professor of Biology and Director of Honors

BS, 1977 & MS, 1988 Iowa State University Ph.D., 1992 Duke University

Postdoctoral Fellowship, Pathology Departments, Brigham & Women's Hospital, Children's Hospital and Harvard Medical School, 1992-1994

Johnson & Johnson Toxicology Scholar Rutgers University, 1994-1997

Research Interests:Developmental Neurobiology, Neurotoxicology, Interactions of the Cytoskeleton

Research Interests:

The research interests of this laboratory are focused on development of the nervous systems in mammals using a combination of basic science and toxicologic research techniques in cultured neurons.

The development of the nervous system is an exquisite process that is both spatially and temporally controlled. The mechanisms that initiate and maintain nervous system development are only beginning to be understood. Cells that are predestined to become neurons must divide to produce adequate numbers of cells, migrate to their final destination, and establish connections with other cells. These connections often require the processes, especially axons, to span long distances. The goals of this laboratory are to study the basic processes involved in the initiation and pathfinding mechanisms of neuronal processes. The cytoskeleton, an interconnected group of proteins within the cytoplasm, plays a major role in these processes and is one of the focal points of our research.

In addition to basic mechanisms the effects of developmental neurotoxicants on the processes of initiation and pathfinding are examined in this laboratory. Drugs of abuse, such as cocaine, have been implicated in long term cognitive deficits in exposed individuals. The effects of this compound on the development of neuronal processes and on the establishment of synaptic connections may help to explain these behavioral affects.

Nicotine is a compound that has been implicated as a risk factor in Sudden Infant Death Syndrome. Initial studies with this compound indicate that it accelerates the process of differentiation in neuronal cells that have nicotinic Acetylcholine receptors. While the mechanisms involved in acceleration of differentiation are not known premature activation of second messenger pathways is implicated in this process. The effects of nicotine on second messenger signalling is another focal point in our research.

Representative Publications:

Jurgens, CWD, Boese, SJ, King, JD, Pyle, SJ, Porter, JE and Doze, VA. "Adrenergic receptor modulation of Hippocampal CA3 network activity," Epilepsy Res., 66:117-28, 2005.

Pyle, SJ, Roberts, KG and Reuhl, KR. "Delayed expression of the NFH subunit in differentiating P19 cells," Dev. Brain Res., 132(1):103-106, 2001.

Pyle, SJ and Reuhl, KR. Cytoskeletal Elements in Neurotoxicity. In: Comprehensive Toxicology. Vol. 11. Eds.: Sipes, I.G., McQueen, C.A., Gandolfi, A.J., Elsevier Science, Ltd., Cambridge, pp. 79-97, 1997.

Graham, DG, Amarnath, V, Valentine, WM, Pyle, SJ and Anthony, DC. Pathogenetic studies of hexane and carbon disulfide neurotoxicity. Crit. Rev. Toxicol. 25:91-112, 1995.

Pyle, SJ, Graham, DG and Anthony, DC. Dimethylhexanedione impairs the movement of neurofilament protein subunits, NFM and NFL, in the optic system. Neurotoxicology 15:279-286, 1994.

Pyle, SJ, Amarnath, V, Graham, DG and Anthony, DC. Decreased levels of the high molecular weight subunit of neurofilaments and accelerated neurofilament transport during the recovery phase of 2,5-hexanedione exposure. Cell Motil. Cytoskel. 26:133-143, 1993.

Pyle, SJ, Amarnath, V, Graham, DG and Anthony, DC. The role of pyrrole formation in the alteration of neurofilament transport induced during exposure to 2,5-hexanedione. J. Neuropathol. Exp. Neurol. 51:451-458, 1992.