J J Eggermont

The University of Calgary, Calgary, Alberta, Canada

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Publications (205)555.96 Total impact

  • Jos J Eggermont
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    ABSTRACT: Ten years ago, animal models of noise-induced hearing loss predicted three cortical neural correlates of tinnitus resulting from noise-induced hearing loss: increased spontaneous firing rates, increased neural synchrony, and reorganization of tonotopic maps. Salicylate also induces tinnitus, however, the cortical correlates were reduced spontaneous firing rates, unchanged neural synchrony but some change to the tonotopic map. In both conditions increased central gain, potentially a correlate of hyperacusis, was found. Behavioral animal models suggested that tinnitus occurred, albeit not in all cases. The study of the neural substrates of tinnitus in humans is currently strongly based on network connectivity using either spontaneous EEG or MEG. Brain imaging combined with powerful analyses is now able to provide in excellent detail the lay out of tonotopic maps, and has shown that in people with tinnitus (and clinical normal hearing up to 8 kHz) no changes in tonotopic maps need to occur, dispensing therefore of one of the postulated neural correlates. Patients with hyperacusis and tinnitus showed increased gain, as measured using fMRI, from brainstem to cortex, whereas patients with tinnitus without hyperacusis only showed this in auditory cortex. This suggested that top down mechanisms are also needed. The open problems can be formulated by the following questions. 1) Are the neural substrates of tinnitus etiology dependent? 2) Can animal results based on single unit and local field potentials be validated in humans? 3) Can sufficient vs. necessary neural substrates for tinnitus be established. 4) What is the role of attention and stress in engraining tinnitus in memory?
    Hearing research. 10/2014;
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    Jos J Eggermont, Larry E Roberts
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    ABSTRACT: Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide. Most cases are associated with hearing loss that may be detected by the audiogram or by more sensitive measures. Converging evidence from animal models and studies of human tinnitus sufferers indicates that, while cochlear damage is a trigger, most cases of tinnitus are not generated by irritative processes persisting in the cochlea but by changes that take place in central auditory pathways when auditory neurons lose their input from the ear. Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations. Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.
    Cell and Tissue Research 09/2014; · 3.68 Impact Factor
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    ABSTRACT: People are increasingly being exposed to environmental noise from traffic, media and other sources that falls within and outside legal limits. Although such environmental noise is known to cause stress in the auditory system, it is still generally considered to be harmless. This complacency may be misplaced: even in the absence of cochlear damage, new findings suggest that environmental noise may progressively degrade hearing through alterations in the way sound is represented in the adult auditory cortex.
    Nature reviews. Neuroscience. 06/2014; 15(7):483-91.
  • Jos J Eggermont
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    ABSTRACT: Human temporal processing relies on bottom-up as well as top-down mechanisms. Animal models thereof, in the vast majority, are only probing the bottom-up mechanisms. I will review the vast literature underlying auditory temporal processing to elucidate some basic mechanisms that underlie the majority of temporal processing findings. Some basic findings in auditory temporal processing can all be based on mechanisms determining perstimulatory adaptation of firing rate. This is based on transmitter release mechanisms in peripheral as well as central synapses. It is surprising that the adaptation and recovery time constants that define perstimulatory firing rate adaptation are not very different between auditory periphery and auditory cortex when probed with similar stimuli. It is shown that forward masking, gap and VOT detection, and temporal modulation transfer functions are all directly related to perstimulatory adaptation, whereas stimulus-specific adaptation is at least partly dependent on it. Species differences and the fact that most of the studies reviewed were done in anesthetized animals need to be taken into account when extrapolating animal findings to human perceptual studies. In addition, the accuracy of first-spike latency plays a major role in sound localization and in the brainstem mechanisms for periodicity pitch and forms the basis for understanding evoked potential studies in humans. These mechanisms are also crucial for determining neural synchrony underlying perceptual binding and some important aspects of stream segregation.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 04/2014; · 3.05 Impact Factor
  • Jos J. Eggermont
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    ABSTRACT: Human temporal processing relies on bottom-up as well as top-down mechanisms. Animal models thereof, in the vast majority, are only probing the bottom-up mechanisms. I will review the vast literature underlying auditory temporal processing to elucidate some basic mechanisms that underlie the majority of temporal processing findings. Some basic findings in auditory temporal processing can all be based on mechanisms determining perstimulatory adaptation of firing rate. This is based on transmitter release mechanisms in peripheral as well as central synapses. It is surprising that the adaptation and recovery time constants that define perstimulatory firing rate adaptation are not very different between auditory periphery and auditory cortex when probed with similar stimuli. It is shown that forward masking, gap and VOT detection, and temporal modulation transfer functions are all directly related to perstimulatory adaptation, whereas stimulus-specific adaptation is at least partly dependent on it. Species differences and the fact that most of the studies reviewed were done in anesthetized animals need to be taken into account when extrapolating animal findings to human perceptual studies. In addition, the accuracy of first-spike latency plays a major role in sound localization and in the brainstem mechanisms for periodicity pitch and forms the basis for understanding evoked potential studies in humans. These mechanisms are also crucial for determining neural synchrony underlying perceptual binding and some important aspects of stream segregation.
    International Journal of Psychophysiology. 01/2014;
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    Jos J Eggermont, Raymundo Munguia, Gregory Shaw
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    ABSTRACT: Here we use a modification of the Joint-Peri-Stimulus-Time histogram (JPSTH) to investigate triple correlations between cat auditory cortex neurons. The modified procedure allowed the decomposition of the xy-pair correlation into a part that is due to the correlation of the x and y units with the trigger unit, and a remaining 'pair correlation'. We analyzed 16 sets of 15-minute duration stationary spontaneous recordings in primary auditory cortex (AI) with between 11 and 14 electrodes from 2 arrays of 8 electrodes each that provided spontaneous firing rates above 0.22 sp/s and for which reliable frequency-tuning curves could be obtained and the characteristic frequency (CF) was estimated. Thus we evaluated 11,282 conditional cross-correlation functions. The predictor for the conditional cross-correlation, calculated on the assumption that the trigger unit had no effect on the xy-pair correlation but using the same fraction of xy spikes, was equal to the conventional pair-wise correlation function between units xy. The conditional correlation of the xy-pair due to correlation of the x and/or y unit with the trigger unit decreased with the geometric mean distance of the xy pair to the trigger unit, but was independent of the pair cross-correlation coefficient. The conditional pair correlation coefficient was estimated at 78% of the measured pair correlation coefficient. Assuming a geometric decreasing effect of activities of units on other electrodes on the conditional correlation, we estimated the potential contribution of a large number of contributing units on the measured pair correlation at 35-50 of that correlation. This suggests that conventionally measured pair correlations in auditory cortex under ketamine anesthesia overestimate the 'true pair correlation', likely resulting from massive common input, by potentially up to a factor 2.
    Hearing research 08/2013; · 2.85 Impact Factor
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    Larry E Roberts, Fatima T Husain, Jos J Eggermont
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    ABSTRACT: Neural mechanisms that detect changes in the auditory environment appear to rely on processes that predict sensory state. Here we propose that in tinnitus there is a disparity between what the brain predicts it should be hearing (this prediction based on aberrant neural activity occurring in cortical frequency regions affected by hearing loss and underlying the tinnitus percept) and the acoustic information that is delivered to the brain by the damaged cochlea. The disparity between the predicted and delivered inputs activates a system for auditory attention that facilitates through subcortical neuromodulatory systems neuroplastic changes that contribute to the generation of tinnitus. We review behavioral and functional brain imaging evidence for persisting auditory attention in tinnitus and present a qualitative model for how attention operates in normal hearing and may be triggered in tinnitus accompanied by hearing loss. The viewpoint has implications for the role of cochlear pathology in tinnitus, for neural plasticity and the contribution of forebrain neuromodulatory systems in tinnitus, and for tinnitus management and treatment.
    Neuroscience & Biobehavioral Reviews 07/2013; · 10.28 Impact Factor
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    R Munguia, M Pienkowski, J J Eggermont
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    ABSTRACT: Changes of neural activity in animal models have been correlated with tinnitus in humans. For instance, increased spontaneous firing rates (SFR), increased spontaneous neural synchrony, and cortical tonotopic map reorganization may underlie this phantom auditory percept. The aim of this study is to quantify the changes in SFR activity in the cat primary auditory cortex, after long-term exposure to different types of non-traumatic acoustic environments. For that purpose, four different groups of adult cats were exposed to moderate-level (∼70dB SPL), behaviorally-irrelevant sounds for several weeks to months, and their SFRs were compared with those in control cats. The sounds consisted of random multi-frequency tone pip ensembles with various bandwidths (2-4kHz, 4-20kHz, and a pair of third-octave bands centered at 4 and 16kHz), as well as a "factory noise". Auditory brainstem response (ABR) thresholds, ABR wave 3 amplitudes at ∼55 and 75dB SPL, and distortion product otoacoustic emission (DPOAE) amplitudes were unaffected by the exposure. However, we found that the SFR decreased within the exposure frequency range and increased outside the exposure range. This increased SFR for units with characteristic frequencies outside the exposure frequency range, which was slow to reverse after the exposure offset, suggests a mechanism for tinnitus in the absence of hearing loss.
    Neuroscience Letters 05/2013; · 2.03 Impact Factor
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    Jos J Eggermont
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    ABSTRACT: There is an almost dogmatic view of the different effects of moderate-level sound stimulation in neonatal vs. adult animals. It is often stated that exposure in neonates results in an expansion of the cortical area that responds to the frequencies present in the sound, being either pure tones or frequency modulated sounds. In contrast, recent findings on stimulating adult animals for a sufficiently long time with similar sounds show a contraction of the cortical region responding to those sounds. In this review I will suggest that most neonatal animal results have been wrongly interpreted (albeit generally not by the original authors) and that the changes caused in the critical period (CP) and in adulthood are very similar. Thus, the mechanisms leading to the cortical map changes appear to be similar in the CP and in adulthood. Despite this similarity, the changes induced in the CP are occurring faster and are generally permanent (unless extensive training paradigms to revert the changes are involved), whereas in adults the induction is slower and a slow recovery (months) to pre-exposure conditions takes place.
    Frontiers in Systems Neuroscience 01/2013; 7:12.
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    ABSTRACT: Persistent, passive exposure of adult cats to bandlimited tone pip ensembles or sharply-filtered white noise at moderate levels (∼70 dB SPL) leads to a long-term suppression of spontaneous and sound-evoked activity in the region(s) of primary auditory cortex (AI) normally tuned to the exposure spectrum, and to an enhancement of activity in one or more neighboring regions of AI, all in the apparent absence of hearing loss. Here, we first examined the effects of passive exposure to a more structured, real-world noise, consisting of a mix of power tool and construction sounds. This "factory noise" had less pronounced effects on adult cat AI than our previous random tone pip ensembles and white noise, and these effects appeared limited to the region of AI tuned to frequencies near the sharp factory noise cutoff at 16 kHz. To further investigate the role of sharp spectral edges in passive exposure-induced cortical plasticity, a second group of adult cats was exposed to a tone pip ensemble with a flat spectrum between 2 and 4 kHz and shallow cutoff slopes (12 dB/oct) on either side. Compared to our previous ensemble with the same power in the 2-4 kHz band but very steep slopes, exposure to the overall more intense, sloped stimulus had much weaker effects on AI. Finally, we explored the issue of exposure stimulus spectrotemporal density and found that low aggregate tone pip presentation rates of about one per second sufficed to induce changes in the adult AI similar to those characteristic of our previous, much denser exposures. These results are discussed in light of the putative mechanisms underlying exposure-induced auditory cortical plasticity, and the potential adverse consequences of working or living in moderately noisy environments.
    Hearing research 11/2012; · 2.85 Impact Factor
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    Martin Pienkowski, Jos J Eggermont
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    ABSTRACT: It has become increasingly clear that even occasional exposure to loud sounds in occupational or recreational settings can cause irreversible damage to the hair cells of the cochlea and the auditory nerve fibers, even if the resulting partial loss of hearing sensitivity, usually accompanied by tinnitus, disappears within hours or days of the exposure. Such exposure may explain at least some cases of poor speech intelligibility in noise in the face of a normal or near-normal audiogram. Recent findings from our laboratory suggest that long-term changes to auditory brain function-potentially leading to problems with speech intelligibility-can be effected by persistent, passive exposure to more moderate levels of noise (in the 70 dB SPL range) in the apparent absence of damage to the auditory periphery (as reflected in normal distortion product otoacoustic emissions and auditory brainstem responses). Specifically, passive exposure of adult cats to moderate levels of band-pass-filtered noise, or to band-limited ensembles of dense, random tone pips, can lead to a profound decrease of neural activity in the auditory cortex roughly in the exposure frequency range, and to an increase of activity outside that range. This can progress to an apparent reorganization of the cortical tonotopic map, which is reminiscent of the reorganization resulting from hearing loss restricted to a part of the hearing frequency range, although again, no hearing loss was apparent after our moderate-level sound exposure. Here, we review this work focusing specifically on the potential hearing problems that may arise despite a normally functioning auditory periphery.
    Ear and hearing 02/2012; 33(3):305-14. · 2.06 Impact Factor
  • Jos J Eggermont
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    ABSTRACT: Animal models of tinnitus require a behavioral correlate thereof. Various conditioned response methods and gap-startle reflex methods are in use and the outcomes generally correspond with putative electrophysiological substrates of tinnitus. However, for salicylate-induced tinnitus there is discordance between the behavioral and electrophysiological test results. As a result, it is not clear what the various tests are reflecting. A review of the, mostly sub-cortical, neural circuits that underlie the behavioral responses suggests that cortical electrophysiological correlates do not necessarily have to correspond with behavioral ones. Human objective correlates of tinnitus point heavily into cortical network, but not just auditory cortex, correlates of tinnitus. Furthermore, the synaptic mechanisms underlying spontaneous firing rate changes may be different from those involved in driven neural activity.
    Hearing research 02/2012; · 2.85 Impact Factor
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    Jos J Eggermont, Larry E Roberts
    Frontiers in Systems Neuroscience 01/2012; 6:53.
  • Martin Pienkowski, Jos J Eggermont
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    ABSTRACT: The distribution of neuronal characteristic frequencies over the area of primary auditory cortex (AI) roughly reflects the tonotopic organization of the cochlea. However, because the area of AI activated by any given sound frequency increases erratically with sound level, it has generally been proposed that frequency is represented in AI not with a rate-place code but with some more complex, distributed code. Here, on the basis of both spike and local field potential (LFP) recordings in the anesthetized cat, we show that the tonotopic representation in AI is much more level tolerant when mapped with spectrotemporally dense tone pip ensembles rather than with individually presented tone pips. That is, we show that the tuning properties of individual unit and LFP responses are less variable with sound level under dense compared with sparse stimulation, and that the spatial frequency resolution achieved by the AI neural population at moderate stimulus levels (65 dB SPL) is better with densely than with sparsely presented sounds. This implies that nonlinear processing in the central auditory system can compensate (in part) for the level-dependent coding of sound frequency in the cochlea, and suggests that there may be a functional role for the cortical tonotopic map in the representation of complex sounds.
    Journal of Neurophysiology 06/2011; 106(2):1016-27. · 3.30 Impact Factor
  • Martin Pienkowski, Jos J Eggermont
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    ABSTRACT: Central topographic representations of sensory epithelia have a genetic basis, but are refined by patterns of afferent input and by behavioral demands. Here we review such experience-driven map development and plasticity, focusing on the auditory system, and giving particular consideration to its adaptive value and to the putative mechanisms involved. Recent data have challenged the widely held notion that only the developing auditory brain can be influenced by changes to the prevailing acoustic environment, unless those changes convey information of behavioral relevance. Specifically, it has been shown that persistent exposure of adult animals to random, bandlimited, moderately loud sounds can lead to a reorganization of auditory cortex not unlike that following restricted hearing loss. The mature auditory brain is thus more plastic than previously supposed, with potentially troubling consequences for those working or living in noisy environments, even at exposure levels considerably below those presently considered just-acceptable.
    Neuroscience & Biobehavioral Reviews 02/2011; 35(10):2117-28. · 10.28 Impact Factor
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    ABSTRACT: We have recently demonstrated that persistent, passive exposure of adult cats to bandlimited tone pip ensembles at moderate intensities (∼70 dB SPL) leads to a long-term suppression of neural activity in auditory cortex, in the absence of hearing loss. With wideband ensembles (4-20 kHz), the suppression is limited to the exposure frequency range; with narrowband ensembles (2-4 kHz, or third-octave bands centered at 4 and 16 kHz), suppression occurs not only within but also well beyond the exposure range, at least in primary auditory cortex (AI). (In secondary cortex (AII) suppression remains limited mostly to the exposure range even for narrowband ensembles.) We report here on two additional experiments. First, we demonstrate suppression in both AI and AII upon exposure to 4-20 kHz bandlimited noise, thus generalizing our previous results obtained with tonal ensembles. However, we found a somewhat different suppression pattern with noise. Whereas 4-20 kHz tone exposure produced relatively uniform suppression over the 4-20 kHz range, save for a small local minimum at ∼10 kHz, 4-20 kHz noise produced maximal suppression over ∼4-10 kHz, which then progressively weakened with frequency up to 20 kHz. Second, we outline the time course of the emergence of response suppression in AI, using the above-mentioned pair of third-octave bands as the exposure stimulus. Suppression emerged relatively rapidly, within a week of exposure onset, and was initially confined to frequencies close to the 4 and 16 kHz stimulus bands. Over the course of several more weeks, the suppression broadened to cover the entire 4-16 kHz range. We discuss these new findings with reference to the putative mechanisms underlying exposure-induced auditory cortical plasticity.
    Hearing research 02/2011; 277(1-2):117-26. · 2.85 Impact Factor
  • Jos J Eggermont
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    ABSTRACT: The spectro-temporal receptive field (STRF) is frequently used to characterize the linear frequency-time filter properties of the auditory system up to the neuron recorded from. STRFs are extremely stimulus dependent, reflecting the strong non-linearities in the auditory system. Changes in the STRF with stimulus type (tonal, noise-like, vocalizations), sound level and spectro-temporal sound density are reviewed here. Effects on STRF shape of task and attention are also briefly reviewed. Models to account for these changes, potential improvements to STRF analysis, and implications for neural coding are discussed.
    Hearing research 01/2011; 271(1-2):123-32. · 2.85 Impact Factor
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    ABSTRACT: Multi-electrode array recordings of spike and local field potential (LFP) activity were made from primary auditory cortex of 12 normal hearing, ketamine-anesthetized cats. We evaluated 259 spectro-temporal receptive fields (STRFs) and 492 frequency-tuning curves (FTCs) based on LFPs and spikes simultaneously recorded on the same electrode. We compared their characteristic frequency (CF) gradients and their cross-correlation distances. The CF gradient for spike-based FTCs was about twice that for 2-40 Hz-filtered LFP-based FTCs, indicating greatly reduced frequency selectivity for LFPs. We also present comparisons for LFPs band-pass filtered between 4-8 Hz, 8-16 Hz and 16-40 Hz, with spike-based STRFs, on the basis of their marginal frequency distributions. We find on average a significantly larger correlation between the spike based marginal frequency distributions and those based on the 16-40 Hz filtered LFP, compared to those based on the 4-8 Hz, 8-16 Hz and 2-40 Hz filtered LFP. This suggests greater frequency specificity for the 16-40 Hz LFPs compared to those of lower frequency content. For spontaneous LFP and spike activity we evaluated 1373 pair correlations for pairs with >200 spikes in 900 s per electrode. Peak correlation-coefficient space constants were similar for the 2-40 Hz filtered LFP (5.5 mm) and the 16-40 Hz LFP (7.4 mm), whereas for spike-pair correlations it was about half that, at 3.2 mm. Comparing spike-pairs with 2-40 Hz (and 16-40 Hz) LFP-pair correlations showed that about 16% (9%) of the variance in the spike-pair correlations could be explained from LFP-pair correlations recorded on the same electrodes within the same electrode array. This larger correlation distance combined with the reduced CF gradient and much broader frequency selectivity suggests that LFPs are not a substitute for spike activity in primary auditory cortex.
    PLoS ONE 01/2011; 6(5):e20046. · 3.53 Impact Factor
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    ABSTRACT: Tinnitus is a phantom sound (ringing of the ears) that affects quality of life for millions around the world and is associated in most cases with hearing impairment. This symposium will consider evidence that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region. This region covers the frequency spectrum of tinnitus sounds, which are optimally suppressed following exposure to band-limited noise covering the same frequencies. Cross-modal compensations in subcortical structures may contribute to tinnitus and its modulation by jaw-clenching and eye movements. Yet many older individuals with impaired hearing do not have tinnitus, possibly because age-related changes in inhibitory circuits are better preserved. A brain network involving limbic and other nonauditory regions is active in tinnitus and may be driven when spectrotemporal information conveyed by the damaged ear does not match that predicted by central auditory processing.
    Journal of Neuroscience 11/2010; 30(45):14972-9. · 6.91 Impact Factor
  • Martin Pienkowski, Jos J Eggermont
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    ABSTRACT: Passive exposure of adult animals to a random ensemble of tone pips band limited between 4 and 20 kHz has been shown to suppress neural activity in primary auditory cortex (AI) to sounds in the exposure frequency range. In the long-term (>3 months), the suppressed neurons can be reactivated by frequencies above and below the exposure range, i.e., tonotopic map reorganization occurs. The suppression can be at least partially reversed after a long period of quiet recovery, as the moderate-level exposure does not impair peripheral hearing. Here we exposed adult cats, for 7-13 weeks without interruption, to two different moderate-level tone pip ensembles, in separate experiments. One exposure stimulus consisted of an octave-wide 2-4 kHz band, which overlaps substantially with the cat vocalization range; the other consisted of a pair of third-octave bands centered at 4 and 16 kHz. We again report a decrease in AI responsiveness in the exposure frequency range, irrespective of the exposure stimulus bandwidth or center frequency, and a slow, partial recovery over a 12-week post-exposure window. In contrast to our previous studies, the suppression in both of the present experiments extended well beyond the exposure frequency range. In particular, following the 4 and 16 kHz experimental acoustic environment, AI activity was strongly suppressed not only in response to frequencies close to the two exposure bands, but also in response to frequencies between the bands, i.e., the results resembled those to a single broadband stimulus spanning the 3-18 kHz range. On the other hand, responses in secondary auditory cortex (AII) were suppressed predominantly around 4 and 16 kHz, with little or no suppression in between.
    Hearing research 09/2010; 268(1-2):151-62. · 2.85 Impact Factor

Publication Stats

6k Citations
555.96 Total Impact Points

Institutions

  • 1987–2014
    • The University of Calgary
      • • Department of Psychology
      • • Department of Physiology and Pharmacology
      Calgary, Alberta, Canada
  • 2013
    • McMaster University
      • Department of Psychology, Neuroscience & Behaviour
      Hamilton, Ontario, Canada
  • 1973–2009
    • Leiden University
      Leyden, South Holland, Netherlands
  • 2006–2008
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 2007
    • University of Texas at Dallas
      Richardson, Texas, United States
    • University of Hamburg
      • Department of Neurophysiology and Pathophysiology
      Hamburg, Hamburg, Germany
  • 2005–2006
    • Claude Bernard University Lyon 1
      Villeurbanne, Rhône-Alpes, France
  • 2001
    • Compumedics
      Charlotte, North Carolina, United States
  • 1992–1999
    • University of California, Los Angeles
      Los Angeles, California, United States
  • 1997
    • St. Marianna University School of Medicine
      • Department of Otolaryngology
      Kawasaki Si, Kanagawa, Japan
    • House Research Institute
      Los Angeles, California, United States
  • 1975–1990
    • Leiden University Medical Centre
      Leyden, South Holland, Netherlands
  • 1986
    • Delft University Of Technology
      • Applied Geophysics and Petrophysics
      Delft, South Holland, Netherlands
  • 1981–1986
    • Radboud University Nijmegen
      Nymegen, Gelderland, Netherlands