Correlated neural activity as the driving force for functional changes in auditory cortex

Eggermont, Jos J.

doi:10.1016/j.heares.2007.01.008

Cited by 78 publications

(55 citation statements)

References 86 publications

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“…Narrowband noise exposure (7 kHz) resulted in unilateral TTS and tinnitus in the same animals that also underwent simultaneous recordings from DCN (Koehler and Shore 2013b). In A1, increased SFRs following noise exposure in cats (Eggermont 2007;Komiya and Eggermont 2000), a documented neural physiological correlate of tinnitus (reviewed by Eggermont 2015), were significantly increased only in the tinnitus bands (Ͻ12 kHz) compared with sham and noise-exposed animals that did not show evidence of tinnitus. A1 SFRs outside the tinnitus bands (Ͼ12 kHz) did not show significant increases in any group.…”

Section: Discussionmentioning

confidence: 97%

Bimodal stimulus timing-dependent plasticity in primary auditory cortex is altered after noise exposure with and without tinnitus

Basura

Koehler

Shore

2015

Journal of Neurophysiology

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Basura GJ, Koehler SD, Shore SE. Bimodal stimulus timingdependent plasticity in primary auditory cortex is altered after noise exposure with and without tinnitus. J Neurophysiol 114: 3064 -3075, 2015. First published August 19, 2015 doi:10.1152/jn.00319.2015.-Central auditory circuits are influenced by the somatosensory system, a relationship that may underlie tinnitus generation. In the guinea pig dorsal cochlear nucleus (DCN), pairing spinal trigeminal nucleus (Sp5) stimulation with tones at specific intervals and orders facilitated or suppressed subsequent tone-evoked neural responses, reflecting spike timing-dependent plasticity (STDP). Furthermore, after noiseinduced tinnitus, bimodal responses in DCN were shifted from Hebbian to anti-Hebbian timing rules with less discrete temporal windows, suggesting a role for bimodal plasticity in tinnitus. Here, we aimed to determine if multisensory STDP principles like those in DCN also exist in primary auditory cortex (A1), and whether they change following noise-induced tinnitus. Tone-evoked and spontaneous neural responses were recorded before and 15 min after bimodal stimulation in which the intervals and orders of auditory-somatosensory stimuli were randomized. Tone-evoked and spontaneous firing rates were influenced by the interval and order of the bimodal stimuli, and in sham-controls Hebbian-like timing rules predominated as was seen in DCN. In noise-exposed animals with and without tinnitus, timing rules shifted away from those found in sham-controls to more anti-Hebbian rules. Only those animals with evidence of tinnitus showed increased spontaneous firing rates, a purported neurophysiological correlate of tinnitus in A1. Together, these findings suggest that bimodal plasticity is also evident in A1 following noise damage and may have implications for tinnitus generation and therapeutic intervention across the central auditory circuit.

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Section: Discussionmentioning

confidence: 97%

Bimodal stimulus timing-dependent plasticity in primary auditory cortex is altered after noise exposure with and without tinnitus

Basura

Koehler

Shore

2015

Journal of Neurophysiology

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“…Although cases of a disruption of seizure inhibition by callosotomy have also been reported (Spencer et al, 1984; Ferbert et al, 1992; Netz et al, 1995), this effect is not as profound as the disruption of the interhemispheric spread of seizures (Bloom and Hynd, 2005). Assuming that it is hypersynchronous firing of neurons in the auditory cortex that represents the neurophysiological correlate of tinnitus (Eggermont and Roberts, 2004; Eggermont, 2007) and that the default transcallosal influence is mainly excitatory, the CC may well facilitate the development and maintenance of tinnitus. The synchronous activity of a population of single units in one hemisphere may be facilitated by the excitatory transcallosal inputs it receives and may in turn facilitate the emergence of one or more descendant synchronized populations via its callosal projection onto the auditory cortex of the respective contralateral hemisphere.…”

Section: Discussionmentioning

confidence: 99%

Structural changes of the corpus callosum in tinnitus

Diesch

Schummer

Krämer

et al. 2012

Front. Syst. Neurosci.

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Objectives: In tinnitus, several brain regions seem to be structurally altered, including the medial partition of Heschl's gyrus (mHG), the site of the primary auditory cortex. The mHG is smaller in tinnitus patients than in healthy controls. The corpus callosum (CC) is the main interhemispheric commissure of the brain connecting the auditory areas of the left and the right hemisphere. Here, we investigate whether tinnitus status is associated with CC volume. Methods: The midsagittal cross-sectional area of the CC was examined in tinnitus patients and healthy controls in which an examination of the mHG had been carried out earlier. The CC was extracted and segmented into subregions which were defined according to the most common CC morphometry schemes introduced by Witelson (1989) and Hofer and Frahm (2006). Results: For both CC segmentation schemes, the CC posterior midbody was smaller in male patients than in male healthy controls and the isthmus, the anterior midbody, and the genou were larger in female patients than in female controls. With CC size normalized relative to mHG volume, the normalized CC splenium was larger in male patients than male controls and the normalized CC splenium, the isthmus and the genou were larger in female patients than female controls. Normalized CC segment size expresses callosal interconnectivity relative to auditory cortex volume. Conclusion: It may be argued that the predominant function of the CC is excitatory. The stronger callosal interconnectivity in tinnitus patients, compared to healthy controls, may facilitate the emergence and maintenance of a positive feedback loop between tinnitus generators located in the two hemispheres.

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“…Although the tuning shift itself does not represent the tinnitus percept, the shift likely does signal enhanced input via lateral connections to tonotopic regions where tinnitus sounds are generated. Input conveyed by lateral connections (which are known to be highly plastic) could be a driving force for enhanced neural synchrony in the affected cortical regions (Eggermont 2007). One mechanism contributing to synchronous network activity may be homeostatic plasticity, which adjusts neural firing thresholds to preserve spiking rates when other sources of input are lost (Turrigiano 2007).…”

Section: Mechanism Of Tinnitus and Rimentioning

confidence: 99%

Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

Roberts

Moffat

Baumann

et al. 2008

JARO

204

215

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Animals exposed to noise trauma show augmented synchronous neural activity in tonotopically reorganized primary auditory cortex consequent on hearing loss. Diminished intracortical inhibition in the reorganized region appears to enable synchronous network activity that develops when deafferented neurons begin to respond to input via their lateral connections. In humans with tinnitus accompanied by hearing loss, this process may generate a phantom sound that is perceived in accordance with the location of the affected neurons in the cortical place map. The neural synchrony hypothesis predicts that tinnitus spectra, and heretofore unmeasured "residual inhibition functions" that relate residual tinnitus suppression to the center frequency of masking sounds, should cover the region of hearing loss in the audiogram. We confirmed these predictions in two independent cohorts totaling 90 tinnitus subjects, using computer-based tools designed to assess the psychoacoustic properties of tinnitus. Tinnitus spectra and residual inhibition functions for depth and duration increased with the amount of threshold shift over the region of hearing impairment. Residual inhibition depth was shallower when the masking sounds that were used to induce residual inhibition showed decreased correspondence with the frequency spectrum and bandwidth of the tinnitus. These findings suggest that tinnitus and its suppression in residual inhibition depend on processes that span the region of hearing impairment and not on mechanisms that enhance cortical representations for sound frequencies at the audiometric edge. Hearing thresholds measured in age-matched control subjects without tinnitus implicated hearing loss as a factor in tinnitus, although elevated thresholds alone were not sufficient to cause tinnitus.

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Correlated neural activity as the driving force for functional changes in auditory cortex

Cited by 78 publications

References 86 publications

Bimodal stimulus timing-dependent plasticity in primary auditory cortex is altered after noise exposure with and without tinnitus

Bimodal stimulus timing-dependent plasticity in primary auditory cortex is altered after noise exposure with and without tinnitus

Structural changes of the corpus callosum in tinnitus

Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

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