Gap encoding by inferior collicular neurons is altered by minimal changes in signal envelope

Barsz, Kathy; Benson, P.; Walton, Joseph P.

doi:10.1016/s0378-5955(97)00173-1

Cited by 33 publications

(34 citation statements)

References 32 publications

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“…Neural correlates of MGT were quantified using the Wilcoxon signed-rank test and composite PSTH method previously described in detail (Barsz et al 1998;see Fig. 1 in Barsz et al 2000;Wilson and Walton 2002).…”

Section: Discussionmentioning

confidence: 99%

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Walton

Barsz

Wilson

2007

JARO

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Perception of complex sounds depends on the encoding of the dynamic and static structures within the ongoing stimulus by the auditory system. Aging has been associated with deficits in both areas, thus, the difficulty that the elderly have in speech comprehension could due to hearing loss, or to a loss of temporal sensitivity, or some combination of both. We investigated the effects of sensorineural hearing loss (SNHL) on neural correlates of temporal resolution by recording the responses of inferior colliculus neurons to a gap detection paradigm. We used C57BL/6 (C57) strain of laboratory mouse, which carries the Ahl deafness gene that initiates a progressive high frequency SNHL beginning at about 2 months of age and rapidly progresses to total deafness by 18 months. We compared gap encoding from inferior collicular neurons from young, normal-hearing C57 mice and middle-aged, hearing-impaired, C57 mice, quantifying minimal gap threshold, and recovery functions. The proportion of unit types, spontaneous rates and degree of monotonicity were comparable between young and middle-aged C57 mice. As expected, single unit thresholds were elevated by 30-40 dB in middleaged C57 mice. However, no significant differences in mean minimal gap thresholds or in the slopes of the gap recovery functions were found between the two age groups. Thus, the results suggest that moderate high frequency SNHL does not affect temporal processing as measured by the gap detection paradigm.

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Section: Discussionmentioning

confidence: 99%

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Walton

Barsz

Wilson

2007

JARO

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Section: Discussionmentioning

confidence: 99%

“…This criterion is similar to that used by Rees and Palmer (1988). There were 8 response types in the sample: on, on-sustained, on-pause, primary-like, sustained, on-off, buildup and inhibitory, defined as in previous studies Le Beau et al, 1996;Wang et al, 1996;Barsz et al, 1998).For each RIF, spike counts were first smoothed using a 3-intensity moving average. Smoothed RIFs were then normalized by subtracting the count at the lowest intensity from each count in the series, and then dividing each result by the greatest count in the series.…”

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confidence: 99%

Reorganization of receptive fields following hearing loss in inferior colliculus neurons

Barsz¹,

Wilson²,

Walton³

2007

Neuroscience

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We explored frequency and intensity encoding in the inferior colliculus of the C57 mouse model of sensorineural hearing loss. Consistent with plasticity reported in the IC of other models of hearing loss, frequency response areas (FRAs) in hearing impaired (HI) mice were broader with fewer highfrequency units than normal-hearing (NH) mice. The broad FRAs recorded from HI mice had lower cutoffs on the low frequency edge of the FRA. Characteristic frequency (CF) and sharpness of tuning (Q10) calculated from the FRA were used to divide the sample into 4 categories: low-CF sharp-FRA, low-CF broad-FRA, high-CF sharp-FRA, and high-CF broad-FRA units. Rate-intensity functions (RIFs) for CF tones and noise were used to determine the minimum and maximum response counts as well as the sound pressure levels resulting in 10%, 50%, and 90% of the maximum spike count. Tone RIFs of broad FRA units were shifted to the right of tone RIFs of sharp FRA units in both NH and HI mouse IC, regardless of the unit CF. The main effects of hearing loss were seen in the noise RIFs. The low-CF broad-FRA units in HI mice had elevated response to noise, and the high-CF sharp-FRA units in HI mice had lower maximum rates, as compared to the units recorded from NH mice. These results suggest that, as the IC responds to peripheral hearing loss with changes in the representation of frequency, an altered balance between inhibitory and excitatory inputs to the neurons recorded from the HI mice alter aspects of the units' intensity encoding. This altered balance likely occurs, at least in part, outside of the IC. Keywords plasticity; sensorineural hearing loss; C57 mouse; intensity encoding; central auditory nervous system Sensorineural hearing loss occurs in almost 10% of the US population. One of the most debilitating side effects of this condition is difficulty with word comprehension, particularly when the listening environment is noisy (Needleman and Crandell, 1995). Treatment of hearing loss includes amplification, but it cannot be assumed that amplification restores normal perception. For instance, hearing loss alters the frequency tuning curves and rate-intensity functions (RIFs) in central auditory neurons (Willott, 1984, Willott, 1986, and these deficits cannot be compensated by simple amplification alone. In addition, the sensitivity of the auditory system of hearing impaired listeners may be altered by long-term amplification. ForCorresponding Author: Joseph P. Walton, Department of Otolaryngology and Neurobiology and Anatomy, University of Rochester Medical School, 601 Elmwood Ave., Rochester, NY 14642, USA, Joseph_Walton@URMC.rochester.edu, PHONE: 585-275-1248, FAX: 585-244-4103. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that durin...

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“…The time of arrival is the most direct of these, and the latencies of sensory neurons accordingly vary with the properties that shape stimulus onset, such as the rise trajectory and stimulus intensity (Heil and Irvine, 1997;Barsz et al, 1998;Galazyuk and Feng, 2001). In addition to timing information, response latencies encode features that are less obviously related to the temporal properties of stimuli.…”

Section: Introductionmentioning

confidence: 99%

“…However, despite this evidence, there has been little focus within the auditory system or other sensory systems on the specific ways that neuromodulators change latencies and whether these vary for different cell types or occur independently from neuromodulatory effects on response strength. In the experiments described here, we addressed these issues by applying serotonin iontophoretically while recording from single neurons in the inferior colliculus (IC), a nucleus in which the stimulus features that influence latency Fuzessery and Hall, 1996;Barsz et al, 1998;Klug et al, 2000;Galazyuk and Feng, 2001;Faure et al, 2003) and the modulation of response properties by serotonin Pollak, 1999, 2001;Hurley et al, 2002Hurley et al, , 2004 have been well studied. With this approach, we characterized serotonergic effects on latency by (1) quantifying serotonergic effects on the latency and precision of spikes, (2) comparing serotoninevoked changes in latency with changes in spike count and other response properties, and (3) determining the dependence of serotonin-evoked latency shifts on features of the stimulus.…”

Section: Introductionmentioning

confidence: 99%

Serotonin Shifts First-Spike Latencies of Inferior Colliculus Neurons

Hurley¹,

Pollak²

2005

J. Neurosci.

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Many studies of neuromodulators have focused on changes in the magnitudes of neural responses, but fewer studies have examined neuromodulator effects on response latency. Across sensory systems, response latency is important for encoding not only the temporal structure but also the identity of stimuli. In the auditory system, latency is a fundamental response property that varies with many features of sound, including intensity, frequency, and duration. To determine the extent of neuromodulatory regulation of latency within the inferior colliculus (IC), a midbrain auditory nexus, the effects of iontophoretically applied serotonin on first-spike latencies were characterized in the IC of the Mexican free-tailed bat. Serotonin significantly altered the first-spike latencies in response to tones in 24% of IC neurons, usually increasing, but sometimes decreasing, latency. Serotonin-evoked changes in latency and spike count were not always correlated but sometimes occurred independently within individual neurons. Furthermore, in some neurons, the size of serotonin-evoked latency shifts depended on the frequency or intensity of the stimulus, as reported previously for serotonin-evoked changes in spike count. These results support the general conclusion that changes in latency are an important part of the neuromodulatory repertoire of serotonin within the auditory system and show that serotonin can change latency either in conjunction with broad changes in other aspects of neuronal excitability or in highly specific ways.

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Gap encoding by inferior collicular neurons is altered by minimal changes in signal envelope

Cited by 33 publications

References 32 publications

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Reorganization of receptive fields following hearing loss in inferior colliculus neurons

Serotonin Shifts First-Spike Latencies of Inferior Colliculus Neurons

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