This project is focused on determining how sound damage influences the expression pattern of neurotrophins and neurotrophin receptors in the adult mouse cochlear nucleus (CN). In order to make this determination, the expression pattern of molecules such as NT-3 and trkC must first be characterized in normally developing postnatal and adult animals. This projected was inspired by previous findings of this laboratory demonstrating that a response of the CN to noise damage is the infiltration of new axons into the damaged area and a body of literature indicating that neurotrophin could mediate such regrowth. Immunohistochemical analyses, using antibodies directed against proteins such as NT-3, trkC, SV-2, and NR1, of postnatal, adult, and noise-exposed adult animals will be conducted and the results compared for similarities and differences. ? ?

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 #
1F32DC006120-01
Application #
6646342
Study Section
Communication Disorders Review Committee (CDRC)
Program Officer
Sklare, Dan
Project Start
2003-02-01
Project End
Budget Start
2003-02-01
Budget End
2004-01-31
Support Year
1
Fiscal Year
2003
Total Cost
$41,608
Indirect Cost
Name
University of Connecticut
Department
Neurosciences
Type
Schools of Medicine
DUNS #
022254226
City
Farmington
State
CT
Country
United States
Zip Code
06030
Feng, J; Bendiske, J; Morest, D K (2012) Degeneration in the ventral cochlear nucleus after severe noise damage in mice. J Neurosci Res 90:831-41
Feng, J; Bendiske, J; Morest, D K (2010) Postnatal development of NT3 and TrkC in mouse ventral cochlear nucleus. J Neurosci Res 88:86-94