Colleen C. Hegg, Assistant Professor1990 B.A., Chemistry, Kalamazoo College
1996 Ph.D., Environmental Toxicology, University of Wisconsin - Madison
1996 - 1999 Postdoctoral Fellow, University of Minnesota-Minneapolis
2000 - 2003 Research Associate; Physiology, University of Utah
2003 - 2006 Research Assistant Professor; Physiology, University of Utah
2006 - present Assistant Professor, Pharmacology and Toxicology, Michigan State University
Research Synopsis
Our research is focused on elucidating the mechanisms of neuroregeneration using the olfactory system as a model. We use a variety of techniques including confocal microscopy, live cell imaging, enzyme immunoassays, immunohistochemistry, luminometry and electrophysiology in whole animal studies, in situ preparations and cell culture. There are two current projects in the lab.
Elucidating the mechanisms of injury-evoked regeneration in the mouse olfactory system
The olfactory neuroepithelium (OE) is often easily damaged as it is in direct contact with airborne pollutants, toxicants, and microbes. Although the olfactory epithelium exhibits a remarkable capacity for regeneration, the signals that lead to increased cell proliferation and neurogenesis after injury are poorly understood. In the central nervous system (CNS), ATP mediates cell proliferation, differentiation, and stimulation of neurotrophic factor synthesis, release, or both in a wide range of cell types. The potential role of ATP, alone or in concert with various signaling molecules, in normal and injury-induced neurogenesis remains to be determined in the OE. My general hypothesis is that noxious insult to the OE triggers an extracellular ATP signaling cascade that initiates regeneration of the neuroepithelium. Identification of factors that control and regulate regeneration will have important implications on injury and repair therapeutics in both olfactory and neuronal tissue.
Glial-Neuronal Interactions in the Peripheral Olfactory System
During the past decade, our understanding of the dynamic integrative capacity of glia has dramatically increased. Glia generate and propagate intracellular calcium signals as waves over long distances in response to synaptic activity. Glial calcium signaling has been implicated in a variety of physiological and pathological processes, including modulation of neuronal synaptic signaling and the multicellular response to localized injury. My preliminary studies show that sustentacular cells, the glial-like component of the olfactory epithelium, are capable of generating calcium waves, and spontaneous increases in intracellular calcium. My long term objective is to understand the precise nature of sustentacular cell signals in response to neuronal activity and the consequence of such signals to neuronal function.
Selected Publications Since 2003
CC Hegg, and MT Lucero. 2006. Purinergic receptor antagonists inhibit odorant-evoked heat shock protein 25 induction in mouse olfactory epithelium. Glia, 53:182-190.
F Vogalis, CC Hegg, and MT Lucero. 2005. Electrical coupling in sustentacular cells of the mouse olfactory epithelium. J. Neurophysiol., 94:1001-1012.
F Vogalis, CC Hegg, and MT Lucero. 2005. Ionic conductances in sustentacular cells of the mouse olfactory epithelium. J. Physiol., 562:785-799.
CC Hegg and MT Lucero. 2004. Dopamine reduces odor- and elevated K+-induced calcium responses in mouse olfactory receptor neurons in situ. J. Neurophysiol., 91:1492-1499.
CC Hegg, E Au, AJ Roskams and MT Lucero. 2003. PACAP is present in the olfactory system and elicits calcium transients in olfactory receptor neurons. J. Neurophysiol., 90:2711-2719.
CC Hegg, D Greenwood, W Huang, P Han and MT Lucero. 2003. ATP differentially modulates odor responsiveness through purinergic receptor activation. J. Neuroscience, 23:8291-301.