Sensory-motor interaction in the primate auditory cortex during self-initiated vocalizations.

Journal Article (Journal Article)

Little is known about sensory-motor interaction in the auditory cortex of primates at the level of single neurons and its role in supporting vocal communication. The present study investigated single-unit activities in the auditory cortex of a vocal primate, the common marmoset (Callithrix jacchus), during self-initiated vocalizations. We found that 1) self-initiated vocalizations resulted in suppression of neural discharges in a majority of auditory cortical neurons. The vocalization-induced inhibition suppressed both spontaneous and stimulus-driven discharges. Suppressed units responded poorly to external acoustic stimuli during vocalization. 2) Vocalization-induced suppression began several hundred milliseconds prior to the onset of vocalization. 3) The suppression of cortical discharges reduced neural firings to below the rates expected from a unit's rate-level function, adjusted for known subcortical attenuation, and therefore was likely not entirely caused by subcortical attenuation mechanisms. 4) A smaller population of auditory cortical neurons showed increased discharges during self-initiated vocalizations. This vocalization-related excitation began after the onset of vocalization and is likely the result of acoustic feedback. Units showing this excitation responded nearly normally to external stimuli during vocalization. Based on these findings, we propose that the suppression of auditory cortical neurons, possibly originating from cortical vocal production centers, acts to increase the dynamic range of cortical responses to vocalization feedback for self monitoring. The excitatory responses, on the other hand, likely play a role in maintaining hearing sensitivity to the external acoustic environment during vocalization.

Full Text

Duke Authors

Cited Authors

  • Eliades, SJ; Wang, X

Published Date

  • April 2003

Published In

Volume / Issue

  • 89 / 4

Start / End Page

  • 2194 - 2207

PubMed ID

  • 12612021

International Standard Serial Number (ISSN)

  • 0022-3077

Digital Object Identifier (DOI)

  • 10.1152/jn.00627.2002


  • eng

Conference Location

  • United States