Lithium increases bcl-2 expression in chick cochlear nucleus and protects against deafferentation-induced cell death.

摘要: Approximately 20–30% of neurons in the avian cochlear nucleus (nucleus magnocellularis) die following deafferentation (i.e. deafness produced by cochlea removal) and remaining show a decrease soma size. Cell death is generally accepted to be highly regulated process involving various pro-survival pro-death molecules. One treatment that has been shown modify expression these molecules chronic administration lithium. The present experiments examined whether lithium can protect from deafferentation-induced cell death. Post-hatch chicks were treated with LiCl or saline for 17 consecutive days, beginning on day hatching. On 17th day, unilateral ablation was performed. Five days surgery, magnocellularis counted stereologically opposite sides same brains. Lithium reduced more than 50% (9.8% as compared 22.4% saline-treated subjects). did not affect number intact side brain. also prevent size, suggesting dissociation between mechanisms involved afferent control size those viability. A possible mechanism lithium’s neuroprotective influence second set subjects. Previous studies suggest molecule, bcl-2, may play role regulating deafferentation. Tissues lithium- subjects using immunocytochemistry. Chronic dramatically increased bcl-2 protein neurons. These data impart its effect altering regulate