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 ratebalance 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.

Loudness Perception in the Domestic Cat: Reaction Time Estimates of Equal Loudness Contours and Recruitment Effects

“…Additional statistical testing confirmed that the post-exposure growth of loudness at high levels did not differ from pre-exposure values (slope = 1, sign test with two tails, MATLAB signtest). The low-level slopes show good agreement with the rate-matching slopes of ventral cochlear nucleus (VCN) chopper units in soundexposed cats (1.73; Cai et al 2009) and the median loudness balance slope from several studies of human recruitment (1.9; Miskolczy-Fodor 1960; Moore and Glasberg 2004;Moore et al 1985;Stillman et al 1993;Zeng and Turner 1991).…”

“…Single-unit studies of the VCN suggest that rate-level functions steepen following sound exposure because of substantial increases in maximum rates (Cai et al 2009). This potential correlate of recruitment is restricted to chopper neurons, which show an average slope of 1.7.…”

Effects of Unilateral Acoustic Trauma on Tinnitus-Related Spontaneous Activity in the Inferior Colliculus

“…Because different neuron types are uniquely affected by acoustic trauma (Cai et al 2009), hyperactivity may be expressed in one output pathway of the cochlear nuclei, but not another. The dorsal cochlear nucleus (DCN) has received notable attention as a source of tinnitusrelated hyperactivity (Zhang and Kaltenbach 1998;Brozoski et al 2002), although similar patterns of neuropathology have been confirmed in the ventral cochlear nucleus (VCN) (Vogler et al 2011).…”

Reliability of distortion-product otoacoustic emissions and their relation to loudness

“…However, there are alternative theories about the underlying cause of loudness recruitment. For example, Heinz et al (2005) and Cai et al (2009) have suggested that changes occur in the auditory system beyond its periphery and that these more central changes are responsible for loudness recruitment. Regardless of its source, loudness recruitment can be examined through measures of loudness (Allen et al, 1990;Hellman and Meiselman, 1993;Buss et al, 1998).…”