Encoding intensity in ventral cochlear nucleus following acoustic trauma: Implications for loudness recruitment

Shanqing Cai, Wei Li D Ma, Eric D. Young

Research output: Contribution to journalArticle

Abstract

Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91-105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261-274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons' responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The rate-balance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.

Original languageEnglish (US)
Pages (from-to)5-22
Number of pages18
JournalJARO - Journal of the Association for Research in Otolaryngology
Volume10
Issue number1
DOIs
StatePublished - Mar 2009

Fingerprint

Hyperacusis
Noise-Induced Hearing Loss
Cochlear Nucleus
Neurons
Ear
Wounds and Injuries
Persons With Hearing Impairments
Cochlear Nerve
Sensorineural Hearing Loss
Cats
Central Nervous System

Keywords

  • Acoustic trauma
  • Auditory nerve
  • Bushy cell
  • Hyperacusis
  • Loudness recruitment
  • Neural encoding
  • Neuroplasticity
  • Primary-like units
  • Rate-level function
  • Sensorineural hearing loss
  • Sound intensity
  • Sound level
  • Stellate cell
  • Ventral cochlear nucleus

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Sensory Systems

Cite this

Encoding intensity in ventral cochlear nucleus following acoustic trauma : Implications for loudness recruitment. / Cai, Shanqing; Ma, Wei Li D; Young, Eric D.

In: JARO - Journal of the Association for Research in Otolaryngology, Vol. 10, No. 1, 03.2009, p. 5-22.

Research output: Contribution to journalArticle

@article{7133fded238e4692bc765e07d5bd2272,
title = "Encoding intensity in ventral cochlear nucleus following acoustic trauma: Implications for loudness recruitment",
abstract = "Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91-105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261-274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons' responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The rate-balance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.",
keywords = "Acoustic trauma, Auditory nerve, Bushy cell, Hyperacusis, Loudness recruitment, Neural encoding, Neuroplasticity, Primary-like units, Rate-level function, Sensorineural hearing loss, Sound intensity, Sound level, Stellate cell, Ventral cochlear nucleus",
author = "Shanqing Cai and Ma, {Wei Li D} and Young, {Eric D.}",
year = "2009",
month = "3",
doi = "10.1007/s10162-008-0142-y",
language = "English (US)",
volume = "10",
pages = "5--22",
journal = "JARO - Journal of the Association for Research in Otolaryngology",
issn = "1525-3961",
publisher = "Springer New York",
number = "1",

}

TY - JOUR

T1 - Encoding intensity in ventral cochlear nucleus following acoustic trauma

T2 - Implications for loudness recruitment

AU - Cai, Shanqing

AU - Ma, Wei Li D

AU - Young, Eric D.

PY - 2009/3

Y1 - 2009/3

N2 - Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91-105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261-274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons' responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The rate-balance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.

AB - Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91-105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261-274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons' responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The rate-balance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.

KW - Acoustic trauma

KW - Auditory nerve

KW - Bushy cell

KW - Hyperacusis

KW - Loudness recruitment

KW - Neural encoding

KW - Neuroplasticity

KW - Primary-like units

KW - Rate-level function

KW - Sensorineural hearing loss

KW - Sound intensity

KW - Sound level

KW - Stellate cell

KW - Ventral cochlear nucleus

UR - http://www.scopus.com/inward/record.url?scp=67349231958&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67349231958&partnerID=8YFLogxK

U2 - 10.1007/s10162-008-0142-y

DO - 10.1007/s10162-008-0142-y

M3 - Article

C2 - 18855070

AN - SCOPUS:67349231958

VL - 10

SP - 5

EP - 22

JO - JARO - Journal of the Association for Research in Otolaryngology

JF - JARO - Journal of the Association for Research in Otolaryngology

SN - 1525-3961

IS - 1

ER -