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Tinnitus: animal models and findings in humans.

Eggermont JJ, Roberts LE - Cell Tissue Res. (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Hotchkiss Brain Institute, and Department of Psychology, University of Calgary, 2500 University Drive N.W, Calgary, AB, Canada, eggermon@ucalgary.ca.

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.

No MeSH data available.


Related in: MedlinePlus

A comparison of the responses to a /ba/–/pa/ continuum (a–c) and early gap (d–f) conditions from the same recording site. Dot displays (left column) and PSTH (middle column) are organized vertically according to VOT or gap duration and horizontally for time since the onset of the leading noise burst. Time windows for evaluation of the PSTHs to the trailing stimulus are selected (between dot lines) according to VOT or gap duration and the latency of peak response for the leading noise burst. Compare in the right panels the average normalized maximum firing rate for the vowel (top) and trailing noise burst after the early gap (bottom) obtained before (filled circles) and after (open circles) the acoustic trauma (±SE). The sigmoid curves provide the best statistical fit to the data. Note that fitted curves for both the /ba/–/pa/ continuum and the early gap condition are shifted toward longer VOT or gap duration. FRmax maximum firing rate. From Tomita et al. (2004)
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Fig2: A comparison of the responses to a /ba/–/pa/ continuum (a–c) and early gap (d–f) conditions from the same recording site. Dot displays (left column) and PSTH (middle column) are organized vertically according to VOT or gap duration and horizontally for time since the onset of the leading noise burst. Time windows for evaluation of the PSTHs to the trailing stimulus are selected (between dot lines) according to VOT or gap duration and the latency of peak response for the leading noise burst. Compare in the right panels the average normalized maximum firing rate for the vowel (top) and trailing noise burst after the early gap (bottom) obtained before (filled circles) and after (open circles) the acoustic trauma (±SE). The sigmoid curves provide the best statistical fit to the data. Note that fitted curves for both the /ba/–/pa/ continuum and the early gap condition are shifted toward longer VOT or gap duration. FRmax maximum firing rate. From Tomita et al. (2004)

Mentions: The abnormal auditory temporal processing hypothesis suggests that it may be important to consider the effects of hearing loss alone on gap detection thresholds, since impaired startle suppression could arise from reduced sensitivity to gaps (impaired temporal processing), as well as from filling-in effects from tinnitus. We (Tomita et al. 2004) showed that noise-induced hearing loss causes a decrease in neural temporal resolution. We investigated the effect of an acute NIHL (5 or 6 kHz at 115–120 dB SPL for 1 h) on the representation of a voice onset time (VOT) and gap-duration continuum in primary auditory cortex of the ketamine-anesthetized cat. Multiple single-unit activity related to the presentation of a /ba/–/pa/ continuum—in which VOT was varied in 5-ms steps from 0 to 70 ms—was recorded from the same sites before and after an acoustic trauma using two 8-electrode arrays. We also obtained data for gaps, of duration equal to the various VOT values, embedded in noise 5 ms after the onset. The changes in the maximum firing rate for /ba/–/pa/ continuum as a function of VOT matched the psychometric function for categorical perception of /ba/–/pa/ modeled by a sigmoid function. An acoustic trauma made the sigmoid fitting functions shallower, and shifted them toward higher values of VOT (Fig. 2). The less steep fitting function may be a neural correlate of an impaired psychoacoustic temporal resolution, because the ambiguity between /ba/ and /pa/ should consequently be increased.Fig 2


Tinnitus: animal models and findings in humans.

Eggermont JJ, Roberts LE - Cell Tissue Res. (2014)

A comparison of the responses to a /ba/–/pa/ continuum (a–c) and early gap (d–f) conditions from the same recording site. Dot displays (left column) and PSTH (middle column) are organized vertically according to VOT or gap duration and horizontally for time since the onset of the leading noise burst. Time windows for evaluation of the PSTHs to the trailing stimulus are selected (between dot lines) according to VOT or gap duration and the latency of peak response for the leading noise burst. Compare in the right panels the average normalized maximum firing rate for the vowel (top) and trailing noise burst after the early gap (bottom) obtained before (filled circles) and after (open circles) the acoustic trauma (±SE). The sigmoid curves provide the best statistical fit to the data. Note that fitted curves for both the /ba/–/pa/ continuum and the early gap condition are shifted toward longer VOT or gap duration. FRmax maximum firing rate. From Tomita et al. (2004)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487353&req=5

Fig2: A comparison of the responses to a /ba/–/pa/ continuum (a–c) and early gap (d–f) conditions from the same recording site. Dot displays (left column) and PSTH (middle column) are organized vertically according to VOT or gap duration and horizontally for time since the onset of the leading noise burst. Time windows for evaluation of the PSTHs to the trailing stimulus are selected (between dot lines) according to VOT or gap duration and the latency of peak response for the leading noise burst. Compare in the right panels the average normalized maximum firing rate for the vowel (top) and trailing noise burst after the early gap (bottom) obtained before (filled circles) and after (open circles) the acoustic trauma (±SE). The sigmoid curves provide the best statistical fit to the data. Note that fitted curves for both the /ba/–/pa/ continuum and the early gap condition are shifted toward longer VOT or gap duration. FRmax maximum firing rate. From Tomita et al. (2004)
Mentions: The abnormal auditory temporal processing hypothesis suggests that it may be important to consider the effects of hearing loss alone on gap detection thresholds, since impaired startle suppression could arise from reduced sensitivity to gaps (impaired temporal processing), as well as from filling-in effects from tinnitus. We (Tomita et al. 2004) showed that noise-induced hearing loss causes a decrease in neural temporal resolution. We investigated the effect of an acute NIHL (5 or 6 kHz at 115–120 dB SPL for 1 h) on the representation of a voice onset time (VOT) and gap-duration continuum in primary auditory cortex of the ketamine-anesthetized cat. Multiple single-unit activity related to the presentation of a /ba/–/pa/ continuum—in which VOT was varied in 5-ms steps from 0 to 70 ms—was recorded from the same sites before and after an acoustic trauma using two 8-electrode arrays. We also obtained data for gaps, of duration equal to the various VOT values, embedded in noise 5 ms after the onset. The changes in the maximum firing rate for /ba/–/pa/ continuum as a function of VOT matched the psychometric function for categorical perception of /ba/–/pa/ modeled by a sigmoid function. An acoustic trauma made the sigmoid fitting functions shallower, and shifted them toward higher values of VOT (Fig. 2). The less steep fitting function may be a neural correlate of an impaired psychoacoustic temporal resolution, because the ambiguity between /ba/ and /pa/ should consequently be increased.Fig 2

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Hotchkiss Brain Institute, and Department of Psychology, University of Calgary, 2500 University Drive N.W, Calgary, AB, Canada, eggermon@ucalgary.ca.

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.

No MeSH data available.


Related in: MedlinePlus