Responses of ventral cochlear nucleus neurons to contralateral sound after conductive hearing loss.

Published

Journal Article

Conductive hearing loss (CHL) is an attenuation of signals stimulating the cochlea, without damage to the auditory end organ. It can cause central auditory processing deficits that outlast the CHL itself. Measures of oxidative metabolism show a decrease in activity of nuclei receiving input originating at the affected ear but, surprisingly, an increase in the activity of second-order neurons of the opposite ear. In normal hearing animals, contralateral sound produces an inhibitory response to broadband noise in approximately one third of ventral cochlear nucleus (VCN) neurons. Excitatory responses also occur but are very rare. We looked for changes in the binaural properties of neurons in the VCN of guinea pigs at intervals immediately, 1 day, 1 wk, and 2 wk after the induction of a unilateral CHL by ossicular disruption. CHL was always induced in the ear ipsilateral to the VCN from which recordings were made. The main observations were as follows: 1) ipsilateral excitatory thresholds were raised by at least 40 dB; 2) contralateral inhibitory responses showed a small but statistically significant immediate decrease followed by an increase, returning to normal by 14 days; and 3) there was a large increase in the proportion of units with excitatory responses to contralateral BBN. The increase was immediate and lasting. The latencies of the excitatory responses were at least 6 ms, consistent with activation by a path involving several synapses and inconsistent with cross talk. The latencies and rate-level functions of contralateral excitation were similar to those seen occasionally in normal hearing animals, suggesting an upregulation of an existing pathway. In conclusion, contralateral excitatory inputs to the VCN exist, which are not normally effective, and can compensate rapidly for large changes in afferent input.

Full Text

Duke Authors

Cited Authors

  • Sumner, CJ; Tucci, DL; Shore, SE

Published Date

  • December 2005

Published In

Volume / Issue

  • 94 / 6

Start / End Page

  • 4234 - 4243

PubMed ID

  • 16093339

Pubmed Central ID

  • 16093339

International Standard Serial Number (ISSN)

  • 0022-3077

Digital Object Identifier (DOI)

  • 10.1152/jn.00401.2005

Language

  • eng

Conference Location

  • United States