Sensorineural Deafness and Seizures in Mice Lacking Vesicular Glutamate Transporter 3

Rebecca P. Seal, Omar Akil, Eunyoung Yi, Christopher M. Weber, Lisa Grant, Jong Yoo, Amanda Clause, Karl Kandler, Jeffrey L. Noebels, Elisabeth Glowatzki, Lawrence R. Lustig, Robert H. Edwards

Research output: Contribution to journalArticlepeer-review


The expression of unconventional vesicular glutamate transporter VGLUT3 by neurons known to release a different classical transmitter has suggested novel roles for signaling by glutamate, but this distribution has raised questions about whether the protein actually contributes to glutamate release. We now report that mice lacking VGLUT3 are profoundly deaf due to the absence of glutamate release from hair cells at the first synapse in the auditory pathway. The early degeneration of some cochlear ganglion neurons in knockout mice also indicates an important developmental role for the glutamate released by hair cells before the onset of hearing. In addition, the mice exhibit primary, generalized epilepsy that is accompanied by remarkably little change in ongoing motor behavior. The glutamate release conferred by expression of VGLUT3 thus has an essential role in both function and development of the auditory pathway, as well as in the control of cortical excitability.

Original languageEnglish (US)
Pages (from-to)263-275
Number of pages13
Issue number2
StatePublished - Jan 24 2008



ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Sensorineural Deafness and Seizures in Mice Lacking Vesicular Glutamate Transporter 3'. Together they form a unique fingerprint.

Cite this