QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, April 1, 2009, 29(13):4210-4217; doi:10.1523/JNEUROSCI.0208-09.2009

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Zeng, C. Articles by Shore, S. Search for Related Content PubMed PubMed Citation Articles by Zeng, C. Articles by Shore, S. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Hearing Disorders and Deafness Hazardous Substances DB KANAMYCIN A

 Previous Article  |  Next Article 

Development/Plasticity/Repair
Cochlear Damage Changes the Distribution of Vesicular Glutamate Transporters Associated with Auditory and Nonauditory Inputs to the Cochlear Nucleus

Chunhua Zeng,¹ Nishant Nannapaneni,¹ Jianxun Zhou,¹ Larry F. Hughes,² and Susan Shore¹

¹Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Michigan 48109-0506, and ²Department of Surgery, Division of Otolaryngology, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9629

Correspondence should be addressed to Susan Shore, Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506. Email: sushore{at}umich.edu

Integration of multimodal information is essential for understanding complex environments. In the auditory system, multisensory integration first occurs in the cochlear nucleus (CN), where auditory nerve and somatosensory pathways converge (Shore, 2005). A unique feature of multisensory neurons is their propensity to receive cross-modal compensation after deafening. Based on our findings that the vesicular glutamate transporters, VGLUT1 and VGLUT2, are differentially associated with auditory nerve and somatosensory inputs to the CN, respectively (Zhou et al., 2007), we examined their relative distributions after unilateral deafening. After unilateral intracochlear injections of kanamycin (1 and 2 weeks), VGLUT1 immunoreactivity (ir) in the magnocellular CN ipsilateral to the cochlear damage was significantly decreased, whereas VGLUT2-ir in regions that receive nonauditory input was significantly increased 2 weeks after deafening. The pathway-specific amplification of VGLUT2 expression in the CN suggests that, in compensatory response to deafening, the nonauditory influence on CN is significantly enhanced. One undesirable consequence of enhanced glutamatergic inputs could be the increased spontaneous rates in CN neurons that occur after hearing loss and that have been proposed as correlates of the phantom auditory sensations commonly called tinnitus.

---

Received Jan. 9, 2009; revised Feb. 20, 2009; accepted Feb. 24, 2009.

Correspondence should be addressed to Susan Shore, Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506. Email: sushore{at}umich.edu

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help