4.1 Article

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

Journal

NEURAL PLASTICITY
Volume 2011, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2011/305621

Keywords

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Categories

Funding

  1. NIH [EY019277, DC003086, DC005409, AG09524]
  2. Deafness Research Foundation
  3. Whitehall Foundation
  4. Alfred P. Sloan Foundation
  5. Burroughs Wellcome Fund
  6. [P30 EY001319]
  7. NATIONAL EYE INSTITUTE [R01EY019277, P30EY001319] Funding Source: NIH RePORTER
  8. NATIONAL INSTITUTE ON AGING [P01AG009524] Funding Source: NIH RePORTER
  9. NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [R01DC003086, P30DC005409, R29DC003086] Funding Source: NIH RePORTER

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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.

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