Abstract

Cochlear functions are subject to modulation by higher auditory centers in the brain via the olivocochlear (OC) efferent system, which is believed to provide protection against noise damage and improve our communication ability in the presence of noise. A development role for the OC efferent has also been suggested by recent works showing that severing the OC efferent bundle in neonatal animals hinders the normal development of the high sensitivity and selectivity of the cochlea. The cellular and molecular mechanisms of the OC efferent function are poorly understood. The long-term goal of our study is to understand the molecular mechanisms of the OC efferent in modulating the activities of afferent fibers and to explore its role in the development of normal cochlear functions. This proposal will focus on one of the two OC efferent systems, the lateral OC (LOC) efferent which forms axodendritic synapses with the radial afferent fibers underneath the inner hair cells. Our overall Hypothesis is that the cholinergic and GABAergic neurotransmission in the LOC

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC004709-02
Application #
6489587
Study Section
Special Emphasis Panel (ZRG1-IFCN-6 (01))
Program Officer
Freeman, Nancy
Project Start
2001-01-15
Project End
2005-12-31
Budget Start
2002-01-01
Budget End
2002-12-31
Support Year
2
Fiscal Year
2002
Total Cost
$349,000
Indirect Cost

  Institution

Name
House Ear Institute
Department
Type
DUNS #
City
Los Angeles
State
CA
Country
United States
Zip Code
90057

  Publications

Chen, Bei; Wang, Yunfeng; Geng, Manying et al. (2018) Localization of Glucose Transporter 10 to Hair Cells' Cuticular Plate in the Mouse Inner Ear. Biomed Res Int 2018:7817453
Qu, Yan; Tang, Wenxue; Dahlke, Ian et al. (2007) Analysis of connexin subunits required for the survival of vestibular hair cells. J Comp Neurol 504:499-507
Ahmad, Shoeb; Tang, Wenxue; Chang, Qing et al. (2007) Restoration of connexin26 protein level in the cochlea completely rescues hearing in a mouse model of human connexin30-linked deafness. Proc Natl Acad Sci U S A 104:1337-41
Tang, Wenxue; Zhang, Yanping; Chang, Qing et al. (2006) Connexin29 is highly expressed in cochlear Schwann cells, and it is required for the normal development and function of the auditory nerve of mice. J Neurosci 26:1991-9
Dulon, D; Jagger, D J; Lin, X et al. (2006) Neuromodulation in the spiral ganglion: shaping signals from the organ of corti to the CNS. J Membr Biol 209:167-75
Stong, Benjamin C; Chang, Qing; Ahmad, Shoeb et al. (2006) A novel mechanism for connexin 26 mutation linked deafness: cell death caused by leaky gap junction hemichannels. Laryngoscope 116:2205-10
Wang, Jianbo; Mark, Sharayne; Zhang, Xiaohui et al. (2005) Regulation of polarized extension and planar cell polarity in the cochlea by the vertebrate PCP pathway. Nat Genet 37:980-5
Sun, Jianjun; Ahmad, Shoab; Chen, Shanping et al. (2005) Cochlear gap junctions coassembled from Cx26 and 30 show faster intercellular Ca2+ signaling than homomeric counterparts. Am J Physiol Cell Physiol 288:C613-23
Zhang, Yanping; Tang, Wenxue; Ahmad, Shoab et al. (2005) Gap junction-mediated intercellular biochemical coupling in cochlear supporting cells is required for normal cochlear functions. Proc Natl Acad Sci U S A 102:15201-6
Peng, Ben-Gang; Ahmad, Shoab; Chen, Shanping et al. (2004) Acid-sensing ion channel 2 contributes a major component to acid-evoked excitatory responses in spiral ganglion neurons and plays a role in noise susceptibility of mice. J Neurosci 24:10167-75

Showing the most recent 10 out of 11 publications