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Associate Professor
Office: 338 Irvine Hall
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The efforts of my laboratory are focussed on understanding how neurons protect themselves from death induced by lack of sensory input (deafferentation). A commonly recognized result of deafferentation is increased intracellular calcium concentration [Ca2+]i which can lead to nerve cell death in many areas of the central nervous system. Since most CNS neurons are not able to regenerate after they die, a loss of neurons results in a loss of function. Understanding the ways that nerve cells can prevent an increase in [Ca2+]i may lead to strategies to prevent the nerve cell death that characterizes such neurodegenerative diseases as Alzheimer's, Parkinson's and Huntington's disease. We use the chick auditory brainstem as an experimental system tostudy deafferentation-induced nerve cell loss. Unilateral cochlea removal leads to degeneration of the auditory nerve and subsequent changes in neurons in the chick cochlear nucleus magnocellularis (NM) on the deafferented side only, leaving the contralateral, unoperated NM to serve as an intra-animal control. Currently we are investigating the role of opioid receptors in regulating fluctuations in [Ca2+]i that occur in NM neurons after cochlea removal.
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