Colleen Hegg

RESEARCH:

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.