Type of Document	Thesis
Author	Bush, Angela Lizette
URN	etd-11112004-101829
Title	Lithium protects neurons from deafferentation-induced cell death
Degree	Master of Science
Department	Psychology, Department of
Advisory Committee	Advisor Name Title Richard Hyson Committee Chair Barbara Licht Committee Member Frank Johnson Committee Member
Keywords	Neuroprotection Cell Death
Date of Defense	2004-11-03
Availability	unrestricted
Abstract Approximately 20-30% of neurons in the avian cochlear nucleus, nucleus magnocellularis (NM) die following deafferentation (i.e., deafness produced by cochlea removal) and there is no known treatment to prevent this cell death. Cell death is generally accepted to be a highly regulated process involving a variety of pro-survival and pro-death molecules. One treatment that has been shown to modify the expression of these molecules is chronic administration of lithium, which has been shown to reduce neuronal death in animal models of neurodegenerative disorders and death induced by ischemia. Cell death following deafferentation has been shown to share some, but not all of the molecular events observed following other death-inducing insults. The present experiment examined whether lithium treatment can protect neurons from deafferentation-induced cell death. Post-hatch chicks were treated with LiCl or saline for 17 consecutive days, beginning on the day of hatching. On the 17th day, a unilateral cochlea ablation was performed to produce cell death on one side of the brain. Chicks were then allowed to survive for 5 days, brains were sectioned coronally, stained for nissl, and the NM neurons were stereologically counted on opposite sides of the same brain. Birds treated with lithium prior to cochlea removal showed only 9% cell death in the deafferented NM (n=8) as compared to approximately 22% cell death observed in the saline treated controls (n=8). Lithium did not affect cell number on the intact side of the brain. We hypothesize that the reliable neuroprotective effect of lithium may result from an up-regulation of pro-survival molecules in NM neurons.
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