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Neural Plasticity
Volume 2011 (2011), Article ID 305621, 12 pages
Research Article

Loss of Prestin Does Not Alter the Development of Auditory Cortical Dendritic Spines

1Program in Neuroscience, Harvard University, Cambridge, MA 02138, USA
2Department of Neurobiology and Anatomy, University of Rochester, Rochester, NY 14627, USA
3Department of Biomedical Engineering, University of Rochester, Rochester, NY 14627, USA
4Department of Brain & Cognitive Sciences, University of Rochester, Rochester, NY 14627, USA
5Center for Visual Science, University of Rochester, Rochester, NY 14627, USA

Received 2 January 2011; Accepted 1 March 2011

Academic Editor: M. B. Dutia

Copyright © 2011 L. J. Bogart et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Disturbance of sensory input during development can have disastrous effects on the development of sensory cortical areas. To examine how moderate perturbations of hearing can impact the development of primary auditory cortex, we examined markers of excitatory synapses in mice who lacked prestin, a protein responsible for somatic electromotility of cochlear outer hair cells. While auditory brain stem responses of these mice show an approximately 40 dB increase in threshold, we found that loss of prestin produced no changes in spine density or morphological characteristics on apical dendrites of cortical layer 5 pyramidal neurons. PSD-95 immunostaining also showed no changes in overall excitatory synapse density. Surprisingly, behavioral assessments of auditory function using the acoustic startle response showed only modest changes in prestin KO animals. These results suggest that moderate developmental hearing deficits produce minor changes in the excitatory connectivity of layer 5 neurons of primary auditory cortex and surprisingly mild auditory behavioral deficits in the startle response.