To date, nearly all in vitro studies examining the role of membrane depolarization on spiral ganglion neuron (SGN) survival have used chronic depolarization as a model. These studies demonstrated the requirement of cytosolic Ca2+ for the neurotrophic effects of depolarization; however, chronic depolarization is an imperfect model of physiological neural activity, which occurs as patterns of brief bursts of depolarization. There is accumulating evidence that different patterns of Ca2+ oscillations result in different patterns of intracellular signaling. Moreover, under conditions of chronic depolarization only a single voltage-gated Ca2+ channel (the L-type channel) is open, while others are inactivated. This suggests that the signaling pathways activated by chronic depolarization and patterned activity may differ. In the present study I test this by examining the effect of patterned activity on SGN survival, determine how these patterns modulate cytosolic Ca2+, and identify the signaling pathways that promote SGN survival. These studies will identify pathways involved with activity-dependent SGN survival. The result will allow the correlation of electrical stimulation patterns used in cochlear implants with their long-term effects on SGN survival in vivo.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32DC007270-03
Application #
7234322
Study Section
Communication Disorders Review Committee (CDRC)
Program Officer
Cyr, Janet
Project Start
2005-06-01
Project End
2008-05-31
Budget Start
2007-06-01
Budget End
2008-05-31
Support Year
3
Fiscal Year
2007
Total Cost
$50,428
Indirect Cost
Name
University of Iowa
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
062761671
City
Iowa City
State
IA
Country
United States
Zip Code
52242