Research Interests
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. We are investigating the role of several signals, including ATP and NPY, in neuroregeneration. 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
Search all publications in the NCBI Journal Database
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.
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.
CC Hegg and MT Lucero. 2003. Dopamine reduces odor- and elevated K+-induced calcium responses in mouse olfactory receptor neurons in situ. J. Neurophysiol. 91:1492-1499.
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Colleen C. Hegg