Broadband onset inhibition can suppress spectral splatter in the auditory brainstem

PLoS One. 2015 May 15;10(5):e0126500. doi: 10.1371/journal.pone.0126500. eCollection 2015.

Abstract

In vivo intracellular responses to auditory stimuli revealed that, in a particular population of cells of the ventral nucleus of the lateral lemniscus (VNLL) of rats, fast inhibition occurred before the first action potential. These experimental data were used to constrain a leaky integrate-and-fire (LIF) model of the neurons in this circuit. The post-synaptic potentials of the VNLL cell population were characterized using a method of triggered averaging. Analysis suggested that these inhibited VNLL cells produce action potentials in response to a particular magnitude of the rate of change of their membrane potential. The LIF model was modified to incorporate the VNLL cells' distinctive action potential production mechanism. The model was used to explore the response of the population of VNLL cells to simple speech-like sounds. These sounds consisted of a simple tone modulated by a saw tooth with exponential decays, similar to glottal pulses that are the repeated impulses seen in vocalizations. It was found that the harmonic component of the sound was enhanced in the VNLL cell population when compared to a population of auditory nerve fibers. This was because the broadband onset noise, also termed spectral splatter, was suppressed by the fast onset inhibition. This mechanism has the potential to greatly improve the clarity of the representation of the harmonic content of certain kinds of natural sounds.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acoustic Stimulation / methods
  • Action Potentials / physiology
  • Animals
  • Auditory Pathways / physiology*
  • Brain Stem / physiology*
  • Electrophysiology / methods
  • Male
  • Models, Biological
  • Neurons / physiology
  • Rats
  • Rats, Wistar
  • Sound
  • Synaptic Potentials / physiology

Grants and funding

Martin Spencer acknowledges postgraduate scholarships from the National Health and Medical Research Council of Australia (NHMRC - 567164 - www.nhmrc.gov.au/) and National Information and Communication Technology Australia (NICTA - www.nicta.com.au/). The work was supported by the Australian Research Council (DP1094830 - www.arc.gov.au/). NICTA is funded by the Australian Government as represented by the Department of Broadband, Communications and the Digital Economy (www.communications.gov.au/) and the Australian Research Council through the ICT Centre of Excellence program. The Bionics Institute acknowledges the support it receives from the Victorian Government through its Operational Infrastructure Support Program (http://www.business.vic.gov.au/grants-and-assistance/programs/medical-research-operational-infrastructure-program). We acknowledge the late Dame Elisabeth Murdoch for funding the original in vivo research on which the present manuscript is based. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.