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Tinnitus disturbs lives and negatively affects the quality of life of about 2% of the adult world population.
AcknowledgmentsThis study was made possible by the Charite - Universitatsmedizin Berlin Research Funds. Pure tone audiogram measured on the left and right ear of the male and female tinnitus patients with hearing loss in the upper frequency range. Tinnitus frequency (A) and tinnitus loudness (B) measured in the right and left ear of the male and female tinnitus patients with hearing loss. Hearing loss measured in the right and left ears of patients with compensated and decompensated tinnitus.
Total TQ scores (A) and scores of the subscale “somatic complaints” (B) measured in patients with left-side, right-side or bilateral tinnitus. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you.
Aspirin, with sodium salicylate as an active ingredient, is one of the most widely used analgesic, anti-inflammatory, and antipyretic drugs (1). Stimuli were generated with hardware from Tucker-Davis Technologies (TDT, Alachua, FL, USA) and software (SigGen, TDT) and presented through a high frequency speaker (Fostex FT28D, Fostex, Tokyo, Japan). The output of the silver ball electrode used to record the CAP was connected to a preamplifier (RA16LA, TDT) using a flexible, low noise cable. The distortion-product otoacoustic emissions (DPOAE) were recorded in a separate group of rats (n = 8) using a Smart DPOAE system (Intelligent Hearing Systems, FL, USA). The graphs and statistical analyses were performed using GraphPad Prism version 5.00 for Windows (GraphPad Software, San Diego, CA, USA) unless otherwise noted. The CAP amplitudes were measured in both groups before and after salicylate injection (Figures 2A–H). The effects of salicylate, ICA-105665 and ICA-105665 plus salicylate on DPOAE (4–24 kHz), are shown in Figures 4 and 5.
Salicylate-induced sensorineural hearing loss is mainly caused by down regulation of the electromotile response of OHCs, which decreases the neural output of cochlea (4–9).
KCNQ2, KCNQ3, and KCNQ5 are co-expressed in many regions of the cochlea (11, 28), including OHCs, spiral ganglion neurons, and the lateral wall of the cochlea (12, 15).
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.
The authors thank Nina Zirke and Theresa Morgenstern for collecting the data.ReferencesJastreboff, PJ.
This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. All protocols were approved by the Institutional Animal Care and Use Committee (IACUC) of the State University of New York at Buffalo that conform to the guidelines issued by the National Institutes of Health.
The bulla of the left ear was exposed and a silver ball electrode was placed on the round window (27). The output of the preamplifier was delivered to a digital signal processing module (RX5-2, Pentusa Base Station, TDT) connected to a computer.
Salicylate treatment caused a large reduction of the CAP amplitude and noticeable threshold shifts. Effects of ICA-105665 on compound action potential (CAP) threshold shifts induced by salicylate (SS).
Salicylate induced a decrease in DPOAE amplitude at all tested frequencies and more changes were found in the high frequencies. The effects of salicylate and ICA-105665 on the amplitudes of distortion-product otoacoustic emissions (DPOAE). Reduction of KCNQ-mediated currents can increase neuronal excitability to epileptogenic levels and cause convulsion (32). This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractNoise-induced hearing loss (NIHL) and resulting comorbidities like subjective tinnitus are common diseases in modern societies. IntroductionA universal characteristic of modern societies, both in developing and developed countries, is the steadily increasing level of noise exposure within our working environments and during leisure time activities (for review see [1]).
To analyze a possible association of the degree of hearing loss with the severity of tinnitus, we have performed a retrospective study using admission data on 531 patients suffering from chronic tinnitus.
This perception can be induced by various dysfunctions on several levels of the peripheral or central auditory pathway [1].
Therefore, enhancing OHC potassium currents could potentially prevent salicylate-induced temporary hearing loss. These perceptual changes have generally been attributed to functional impairments in the cochlea such as a down regulation of the electromotile response of outer hair cells (OHCs) and a decrease in neural output of the cochlea (4–9). KCNQ4 channels are expressed on hair cells and spiral ganglion neurons (13, 14) and the mutation of KCNQ4 accounts for human non-syndromic deafness DFNA2 an autosomal dominant hearing loss (15). Body temperature was measured and maintained using a heating pad (Homeothermic blanket control unit, Harvard Apparatus, MA, USA). Stimuli were calibrated using a sound level meter (824, Larson Davis, Depew, NY, USA) with a half inch microphone (Larson Davis, model #2559). Since ICA-105665 also caused an increase of DPOAE amplitude, our study suggests that ICA-105665 can compensate for salicylate-induced hearing loss presumably by enhancing the electromotility of OHC through activating potassium currents. ICA-105665 may be a useful compound in protecting against ototoxicity and noise exposure by enhancing the OHC motility. A substance shown to be effective against NIHL in an animal model is the Ginkgo biloba extract EGb 761. Consequently, an increasing number of people suffer from hearing disorders that result from an overexposure to noise, that is, noise-induced hearing loss (NIHL).
We have found that 83% of our tinnitus patients had a high frequency hearing loss corresponding to a noise-induced hearing loss (NIHL). Regardless of the original cause, all patients complain of hearing a tinnitus tone on either one (unilateral) or both sides (bilateral) of the head or ears. The effect of salicylate on OHC electromotility at a high concentration (>1 mM) is likely due to its competition for the chloride anion binding site on the prestin motor protein, rather than plasma membrane mechanics (7).
Since the resting potential of OHC is dependent on potassium currents, KCNQ4 mutation can reduce IK, which leads to selective degeneration of OHCs (16).
After ICA-105665 plus salicylate treatment, the DPOAE amplitudes were significantly larger than those in the salicylate alone group at 16 and 24 kHz (40–60 dB SPL). Treatment with ICA-105665 prior to salicylate injection lessened the SS-induced DPOAE reductions at high frequencies. These currents can be activated at more depolarized potentials than other voltage-gated K+ channels and may be involved in maintaining auditory excitability.
Further effects of the extract on the cellular and systemic levels of the nervous system make it a promising candidate not only for protection against NIHL but also for its secondary comorbidities like tinnitus. Statistical data show that in 2000 about 9% of the general population in the USA display hearing impairments [2]. Depending on the case, tinnitus tone may have low, medium or high frequency and be either relatively quiet (0–3 dB), going up to relatively loud (more than 16 dB). In addition, KCNQ2 is expressed in the modiolus and organ of corti, synaptic regions under hair cells, spiral ganglion auditory neurons, and nerve fibers innervating hair cells (12). Since the peak concentration of ICA-105665 occurred ~1 h after the injection (manuscript in preparation), ICA-105665 was always injected 1 h before salicylate treatment.
Unlike other anti-seizure drugs such as retigabine, which also potentiate GABAa receptor response at slightly higher concentrations, ICA-105665 is more selective and does not affect GABAa receptor responses (33). Following an earlier study we here tested the potential effectiveness of prophylactic EGb 761 treatment against NIHL and tinnitus development in the Mongolian gerbil. Similar data were published for Germany in 2006, where 8% of the 18- to 79-year-old adults appear to be hearing impaired [3]. Interestingly, patients suffering from decompensated chronic tinnitus had a greater degree of hearing loss than the patients with compensated form of tinnitus. Tinnitus may take acute (up to 3 months), sub-acute (4–12 months) or a chronic turn (longer than a year). ICA-105665 also prevented the salicylate-induced reduction of distortion-product otoacoustic emission. This subsequently may depolarize the OHC, which would reduce the net driving force of the transduction current thereby diminishing OHC electromotility. The enhancements of DPOAE amplitude by ICA-105665 were significant at high, but not low frequencies. We monitored the effects of EGb 761 and noise trauma-induced changes on signal processing within the auditory system by means of behavioral and electrophysiological approaches. In addition, we demonstrate that the degree of hearing loss positively correlates with the two subscales (“intrusiveness” and “auditory perceptional difficulties”) of the Tinnitus Questionnaire. Regarding the level of disturbance, tinnitus can be classified as compensated (low-level distress) or decompensated (high-level distress) [2].
A modified version of tinnitus retraining therapy: observing long-term outcome and predictors. Thus, there are at least two mechanisms by which salicylate can cause an OHC-based cochlear hearing loss. The slopes of the DPOAE amplitude–intensity functions were used for statistical analysis.
This suggests that more KCNQ channels are expressed in the basal than the apical turn of cochlea. In our preliminary studies, we also found that ICA-105665 can directly affect the firing properties of neurons in the auditory cortex and the inferior colliculus. We found significantly reduced NIHL and tinnitus development upon EGb 761 application, compared to vehicle treated animals.
Our retrospective study provides indirect evidence supporting the hypothesis that the degree of noise-induced hearing loss influences the severity of tinnitus. The major problem in patients with decompensated tinnitus is sleep interference, because the tinnitus tone keeps the patients awake. M-currents are low-threshold depolarization-activated potassium currents that can be inhibited by the cholinergic agonist muscarine (22).

The expression of KCNQ4 in the IHCs and spiral ganglion neurons decreased from the base to the apex of the cochlea (13). However, ICA-105665 failed to reduce salicylate-induced hyperexcitability in the auditory cortex, which suggests that ICA-105665 and salicylate may target different receptors and channels in the central auditory system (data not included). These protective effects of EGb 761 were correlated with changes in auditory processing, both at peripheral and central levels.
As the prevalence of hearing impairments increases with age, it appears to be sensible to assume that when these children grow up the number of patients with hearing impairments will increase dramatically in the future. Other diseases that follow include depression, a variety of phobias, anxiety disorders, problems with concentration and in extreme cases—suicide. M-currents play a role in stabilizing the resting membrane potential, which is important for regulating cellular excitability and K+ homeostasis (23). Figure 5 showed that after ICA-105665 treatment, the DPOAE amplitude showed a slight increase.
However, there is no report on the gradient of KCNQ2, KCNQ3, or KCNQ5 expression in the cochlea. We propose a model with two main effects of EGb 761 on auditory processing, first, an increase of auditory brainstem activity leading to an increased thalamic input to the primary auditory cortex (AI) and second, an asymmetric effect on lateral inhibition in AI.
Furthermore, as hearing loss may be etiologically responsible for the development of a number of secondary diseases, like hyperacusis (for review see [5]), tinnitus [6, 7], or depression due to social isolation [8], the problem of NIHL should be of immensely growing importance.
Approximately 30 per 100 adults experience tinnitus, whereas about 1–5 persons per 100 suffer from tinnitus and seek medical help [3,4]. The recently identified KCNQ5 channels, often co-expressed with KCNQ3 channels, are expressed in the synaptic endings in the auditory brainstem and the calyx terminals of type I vestibular hair cells (24). This difference was likely caused by the effect of ICA-105665, which enhanced the amplitude of DPOAE.
In this context, two main types of strategies are conceivable: reducing noise exposure by technical measures or preventing the development of NIHL via pharmacological interventions. In the Western world, tinnitus has a big economic impact [5].The onset of tinnitus can have various basis such as neurologic, traumatic, infectious or drug-related [6], however, the major cause of tinnitus is a hearing loss [5].
There was no significant difference at 4 kHz on 1 and 2 h, and 16 kHz on 1 h treatment (Table 1).
Whereas many technical measures, for example, for noise reduction in working environments or public, have the advantage that they may be effective for a large number of people, they are often very expensive and have no effect if the source of noise is self-inflicted [10].During the last few years a large number of substances have been tested both in animal and human studies in search of a powerful drug that is able to prevent NIHL. Hearing loss is usually caused by the aging process (presbycusis) or by the overexposure to noise (noise-induced hearing loss, NIHL).
Based on their physiological mechanisms of effectiveness against NIHL, a number of substance classes may be distinguished. Occupational noise, together with environmental noise pollution, are two major factors contributing to the NIHL [7]. Among these, antioxidants that reduce oxidative stress by elimination of reactive oxygen species (ROS) [11], glucocorticoids, and substances that improve cochlear blood flow (for review see [12]), activate inhibitory transmitter systems [13], or block apoptosis pathways in hair cells were most successfully employed (for review see [14]).A substance that has been shown to protect against NIHL in guinea pigs is the Ginkgo biloba extract EGb 761 [15, 16]. Stange and coworkers demonstrated that animals which were treated with EGb 761 before exposing them to different types of noise trauma exhibited a smaller reduction in auditory nerve compound action potentials (CAP) than untreated controls. These, and a lot of other data, strongly indicate coexistence of both hearing dysfunctions. EGb 761 is a plant extract that is composed of about 80 different compounds which deploy not only one but also a number of different mechanisms presumed to counteract the development of NIHL.
Based on the above data we put forward a hypothesis that the degree of hearing loss could negatively influence the severity of tinnitus.To test our hypothesis we used a retrospective study using data acquired from 531 tinnitus patients.
Well-documented are the protection of neuronal mitochondrial ATP synthesis in the presence of oxidative stress [17, 18], the protection of erythrocyte membranes against oxidative damage, which results in reduced blood viscosity and improved blood flow [19, 20], and neuroprotection through antiapoptotic properties [21–25]. This data were randomly collected on the admission of patients who reported to the day ward of Tinnitus Center at the Charite - Universitatsmedizin in Berlin between January 2008 and March 2010.
In addition, the extract displays a number of effects that may counteract the development of secondary consequences of NIHL like tinnitus. These include increased extracellular dopamine levels in the prefrontal cortex [26], which may reduce depressive behavior that may foster the development of tinnitus [27], by partial inhibition of the norepinephrine transporter [28] or adult neurogenesis of hippocampal neurons [29], which additionally could both lead to cognition increasing effects.
Therefore, EGb 761 is a promising candidate substance for protective measures against NIHL and its consequences.As detailed above, one of the consequences of NIHL may be the development of a tinnitus percept. ParticipantsWe have obtained the data from 531 tinnitus patients (sub-acute and chronic) admitted to a 7-day multimodal tinnitus therapy. In a previous study we have described the development of noise trauma-induced tinnitus in the Mongolian gerbil both on a behavioral and neurophysiological level [31]. We were able to detect a number of neuroplastic changes in auditory brainstem and cortex that were correlated with the development of a tinnitus percept as tested with a well-characterized behavioral paradigm [32]. In particular we could demonstrate a neuronal predisposition for the development of tinnitus. We were able to show that animals developing such a mispercept after an acoustic trauma show significantly less cortical activity already in the healthy state compared to tinnitus-resistant animals.
The latter animals are able to counteract tinnitus development after noise trauma while animals without this ability develop a chronic tinnitus percept.While studies in humans with different Ginkgo biloba extracts so far failed to show any reliable effect on tinnitus perception when given after its development [34, 35], we here tested the effectiveness of a prophylactic treatment with EGb 761 in the context of NIHL and tinnitus development in this animal model. We describe the effects of the EGb 761 extract on the behavioral level (acoustic startle response (ASR) audiometry), the auditory brainstem level (electrophysiological recordings of auditory brainstem responses (ABR)), and the central level (electrophysiological recording of local field potentials (LFP) and single and multiunit responses in auditory cortex (AC)). Our results point to massive neuroplastic effects of EGb 761 on auditory processing both at the peripheral and central level. In addition, tinnitus frequency (kHz) and tinnitus loudness (dB HL) were matched for each patient.
These changes in processing may underlie the observed protective effects against NIHL and in the consequence tinnitus development.2. Psychometry (Tinnitus Questionnaire)Tinnitus-related distress was assessed using validated standard German version of the tinnitus questionnaire (TQ). Influence of environmental factors on the evolution of industrial noise-induced hearing loss.
Ethics Statement and AnimalsMongolian gerbils (Meriones unguiculatus) were housed in standard animal racks (Bio A.S. The TQ is composed of 52 items allocated to six scales: emotional distress, cognitive distress, intrusiveness, auditory perceptual difficulties, sleep disturbances and somatic complaints [12]. The severity level of tinnitus was assigned as “compensated” (low-level distress) with TQ score ? 46 points and “decompensated” (high-level distress) with TQ score > 46 points. Spearman's rank correlation was used to test the statistical relationship between hearing loss and tinnitus parameters or tinnitus severity.
Predominant Number of Patients with Chronic Tinnitus Has a Hearing LossOf all 531 tinnitus patients tested, 441 (83%; 220 men and 221 women) had a hearing loss in the upper frequencies (Figure 1), corresponding to a pattern found in the NIHL [13].
Assessing audiological, pathophysiological and psychological variables in tinnitus patients with or without hearing loss. Two weeks prior to trauma (yellow bar) oral application of vehicle or EGb 761 was performed on a daily basis. There were no significant differences in the hearing loss between the left and the right ear and between male and female patients in this group. Pretrauma measurements included behavioral startle responses (turquoise; hearing threshold and gap-noise tinnitus paradigms), ABR measurements (dark green), and electrophysiological recordings in auditory cortex (light green) both under anesthesia. After the acoustic trauma the measurements were repeated within the first seven days after the trauma.During the oral administration the measurements were started (cf. The mean age of tinnitus patients with NIHL-like audiogram was 50 years (SD = 13, min 16, max 79), with patients most frequently ranging between 40–60 years of age. These included the behavioral testing in the first week of application, the pretrauma auditory brainstem response (ABR) measurements, and the pretrauma recording from the AC within the second week of substance administration.
Tinnitus Characteristics in Patients with Hearing LossOf 441 tinnitus patients with NIHL-like audiogram, 319 patients had pure tone tinnitus whereas 122 patients had noise tinnitus.
The values did not differ between female and male patients except for the subscale “somatic complaints” with woman having significantly greater scores than the male patients (Table 1). Of the 441 patients, 335 patients suffered from compensated tinnitus (TQ ? 46 points) and 106 patients suffered from decompensated tinnitus (TQ > 46 points). For obtaining the behavioral hearing thresholds we used a PPI of ASR paradigm in all animals. 3.4 The Degree of Hearing Loss Correlates with Some of the Psychometric Parameters Measured by TQHearing loss was of significantly higher degree in patients with decompensated tinnitus than in patients with compensated tinnitus (Figure 3).
This means that tinnitus patients with greater hearing loss experience higher tinnitus-related distress. This procedure was performed before the acoustic trauma and during the week after that event. We found no correlation between tinnitus frequency or loudness and distress caused by tinnitus. The evaluation was performed independently by the principal investigator and a technical assistant, who was blind to the state of the animal. Influence of Age on the Psychometric ScoresOur recent study [14] revealed that the age of patients may influence their TQ values. Consequently, in the present study, we have subdivided the patients into three age groups and analyzed their TQ scores as a function of age. We made sure that the animals were always (pre- and posttrauma = trauma status) responding to the 90 dB SPL startle stimulus (cf. For validation of the PPI effect of the prestimuli we performed 1-factiorial ANOVAs for the valid response amplitudes dependent on the prestimulus intensity for each frequency and trauma status separately for each individual animal. Influence of Tinnitus Lateralization on the Psychometric ScoresWe compared the tinnitus-related distress between the patients with left-sided, right-sided and bilateral tinnitus. The mean responses of all 36 animals (19 V, 17 E) before and after trauma are given in Figure 2.
Responses in this threshold paradigm were fitted with a sigmoidal Boltzmann functions for each frequency, trauma status, and animal separately.
DiscussionOur present work was aimed at analyzing the association between noise, the grade of the noise-induced hearing loss and the severity of tinnitus. Our results partially corroborate the findings of others by demonstrating a strong bond between the noise-induced hearing loss and tinnitus [10]. In fact, we have shown that 83% of patients with chronic and sub-acute forms of tinnitus have a high-frequency hearing loss, which is a substantially higher percentage than the 57% reported by Savastano or the 63% reported by Martines et al. The left panel documents the mean hearing thresholds with their 95% confidence interval for clicks and all tested tone frequencies with the -statistics of the interaction of the 2-factorial ANOVA.

The center panel depicts the 1-factorial part of the same ANOVA with the factor group (mean values over all tested frequencies and click).
The sample size in all studies was roughly similar, as were the age and gender distribution. Right panels show the same data separated into animals that do not develop a tinnitus percept (upper panel) and those that did show a tinnitus percept after the trauma (lower panel). However, there was a major difference in the duration of tinnitus between our and the other studies. In the Savastano study, 49% of tinnitus patients had suffered from tinnitus for a time shorter than one year – a group classified as acute and sub-acute tinnitus. The grey area in the left panel indicates significant hearing loss (single sample -test versus 0) in both groups (, ), which is also significant if averaged over all tested frequencies and the click stimulus (center panel, asterisks).
Note that relative changes of thresholds measured with either ABR or ASR have been demonstrated to be identical [33].
Based on the above evidence, one is tempted to cautiously speculate that the tinnitus associated with hearing loss has a greater chance of chronification than the tinnitus without hearing loss. In the other study, Attias and colleagues have indentified a subgroup of patients with tinnitus, who were actively looking for a remedy. The rational of these paradigms is that an animal that perceives tinnitus would be impaired in gap detection because it would hear its own tinnitus within the silent gap (cf. Consequently, when using a gap as prepulse, animals with tinnitus should produce smaller PPI of ASR than animals without tinnitus (cf. Our study gives a base for the explanation of how the degree of noise-induced hearing loss indirectly affects the severity of tinnitus by influencing negatively the loudness of tinnitus.
In agreement with this, the degree of hearing loss correlated positively with two subscales (“intrusiveness” and “auditory perceptional difficulties”) of the Tinnitus Questionnaire. If tinnitus is detected, the different tone frequencies and noise spectra used should give a rough estimate of the spectral content of the tinnitus percept. These particular items of TQ regard the ability to communicate, which is an integral part of the quality of life. Each frequency and gap-condition were repeated 15 times and each test was performed before and after the acoustic trauma. Again the data obtained were checked by eye by the same two experimenters as above via a custom-made Matlab program. With the increased distress of tinnitus, patients withdraw from their normal social life and avoid contacts with others, consistent with the decompensated form of tinnitus.
Interestingly, we found that the patients suffering with decompensated tinnitus had a greater degree of hearing loss than the patients with compensated tinnitus.Noise pollution and occupational noise were demonstrated to induce asymmetric hearing loss, with the left side being affected more than the right one [13]. This approach allowed the determination of a possible frequency-specific tinnitus-related behavior at one octave precision.
Although our analyses demonstrated no statistically significant differences in the hearing loss between the left and the right sides, we found that left-sided tinnitus is more distressing than the right-sided one. Moreover, patients with the left-sided tinnitus had more complaints in the somatic subscale than the right-sided tinnitus patients. After the trauma only a part of the animals showed an undisturbed gap-effect at all frequencies tested while other animals showed no gap-effect at some but not all frequencies (cf. This could be attributed to neuroanatomic differences between the left and right parts of the auditory system.Noise—either occupational or environmental noise pollution—is a major preventable cause of the hearing loss and therefore of chronic tinnitus. Figure 4) which gave a first hint of a possible tinnitus percept but was not yet used as the final classification of the animals in the tinnitus or nontinnitus group (cf. The consequences of noise exposure last for life, as the sensory auditory epithelium never regenerates. The price to pay for the noise exposure includes not only a limited ability to hear but also increased chance to develop chronic decompensated tinnitus, which separates the affected persons from normal social activities and significantly decreases the quality of life.
To avoid possible effects of the acoustic trauma on different stimulation frequencies all startle response data were normalized to minimize variance of the response amplitudes. ConclusionsOur study demonstrates that the chain of events started by overexposure to noise not only induces the hearing loss but also tinnitus with its co-morbidities, finally resulting in a decreased quality of life. Thus we were able to control for differences in the startle amplitudes resulting from the hearing loss at the trauma frequency.
This normalization also guarantees that the reduced ASR response after acoustic trauma is not due to hearing loss rather than a tinnitus percept [39]. Finally, the PPI of ASR in the healthy animal (before trauma) and after the trauma was calculated and the change in PPI relative to pretrauma (in %) was tested against 0 (no change) for each frequency separately with a -test (). Significant positive values for PPI change reflect impaired PPI and therefore indicate the development of a tinnitus percept. Only such animals were therefore classified as probably perceiving tinnitus (T groups) that showed at least one impaired frequency after the trauma independent of the affected frequency itself. As it turned out, in all cases where tinnitus was detected according to one of the two gap-ASR paradigms used, the second gap-ASR paradigm was also positive for tinnitus. Animals without such a significant increase in PPI change were classified as nontinnitus perceiving animals (NT groups) (cf. As it turned out, animals classified as T or NT based on these behavioral measures also differed in neurophysiological response measures (ABR and AC; for example, Figures 7 and 12), thereby strengthening the classification (cf. The upper two animals received the vehicle and the lower two animals received the EGb 761 extract before the trauma. In other cases (KS 42 and KS 07) gap detection was impaired and did not show any significant change after the trauma at least at some frequencies; this was a first indication of T categorization (cf. 2-factorial ANOVA (only interaction shown) depict the changes in no-gap and gap conditions before and after trauma.
Note that even when gap-effects are small on the group level they were always significant in the single animals before trauma. Significant positive values of PPI change reflect an impaired PPI, indicating the development of a tinnitus percept. 2-factorial ANOVA indicates that EGb 761 treated animals develop tinnitus percepts at lower frequencies than vehicle treated controls. Asterisks below or above the abscissa indicate significant change of PPI (-test versus 0): , . To obtain ABR-based audiograms the mean ABR waves were compared to the mean amplitude 200 to 100 ms before the stimulus (baseline). Thresholds were defined automatically by a custom-made Matlab program at the highest attenuation at which the evoked amplitude raised over 2 standard deviations of the baseline; data were discarded at frequencies where this procedure was not possible, for example, at low signal to noise ratios. For additional analysis the root mean square (RMS) value of the ABR signal was calculated from 1 to 5 ms after stimulus onset. For further analysis data from both ears of each animal were used.As behavioral audiograms using PPI of ASR (cf. We have demonstrated earlier [33] that these different methods to assess audiograms in our animal model yield different absolute thresholds but identical relative shifts in hearing thresholds after noise trauma.
Electrophysiological Unit Recordings in Primary Auditory Cortex (AI)In a subset of the 36 animals (3 vehicle, 4 EGb 761) used in this study we performed electrophysiological recordings in auditory cortex in addition to the behavioral and ABR measurements described above. Two to three days after obtaining baseline ASR and ABR data, that is, before the acoustic trauma, the skull of the anesthetized animals was trepanned to expose the left auditory cortex. In addition to these iso-intensity measurements, tuning curves were recorded using pure tones in the mentioned frequency range but at different intensities ranging from 0 to 90 dB SPL. The recorded unit activity was analyzed with custom-made Matlab and IDL programs (IDL 7.06, Exelis Visual Information Solutions, McLean, VA, USA).
Where appropriate, either parametric statistics (Student's -test, one- and two-factorial ANOVA with Tukey post-hoc-test) or nonparametric statistics (Kolmogorov-Smirnov-test, Kruskal-Wallis ANOVA with post hoc Median-test, and Mann-Whitney -test) were applied.3.
Effects of Prophylactic EGb 761 Treatment on NIHL and Tinnitus EmergenceWe used the PPI of the ASR to obtain behavioral audiograms from all 36 animals before and after the acoustic trauma. The responses to the different prestimulus intensities were checked by 1-factorial ANOVAs for each frequency and trauma status (before or after trauma) and for each individual animal separately. For an overview of the different response characteristics before and after trauma the mean response amplitudes of the 19 vehicle treated and 17 EGb 761 treated animals are given in Figure 2. Note that we find different response characteristics dependent on the stimulation frequency and trauma status but always find the significant prestimulus intensity effect of the PPI, that is, a decrease in ASR amplitude with increasing prestimulus intensity, which is not only true for the mean response but also for the individual responses. To these individual responses we fitted sigmoidal Boltzmann functions obtaining the individual behavioral hearing thresholds for each frequency.Additional to these behavioral thresholds we obtained individual ABR based hearing thresholds under anesthesia before and after the trauma. Nevertheless, the impact of the trauma on the hearing thresholds was significantly stronger in group V compared to group E (Figure 3(b) center).
Furthermore, the degree of NIHL that developed differed between the V and E groups during the first week after trauma (Figures 3(c) and 3(d)). Whereas the frequency specificity of the NIHL vanished in both groups resulting in flat NIHL functions, the overall threshold shift completely recovered in group E, resulting in audiograms not significantly different from pretrauma conditions 7 days after trauma. The temporal development was entirely different between NT and T animals (Figures 3(c) right, 3(d) right). While NT animals showed no remaining hearing loss only 1 day after trauma, all vehicle treated animals and the T animals of the E group showed increased NIHL until day 7 after trauma. Note that we show the relative hearing loss compared to pretrauma level as we want to keep the two different methods of hearing threshold level measurements comparable. As we have demonstrated in an earlier study [33] ABR and ASR thresholds differ in absolute values so that audiograms show a parallel upward or downward shift. Relative changes due to hearing loss on the other hand were identical for both methods.As described above, both EGb 761 and vehicle treated groups contained T and NT animals.
Exemplarily the mean response amplitudes to both gap-ASR paradigms of four animals are depicted in Figure 4. The two upper animals were treated with the vehicle and the two lower ones with the substance. In animals KS 51 and KS 16 significant gap detection (-tests, ) was found before and after the trauma at all frequencies tested. This impairment was a first hint for the classification of these two animals into the tinnitus group (cf. The mean startle response amplitudes for all these animals before and after the acoustic trauma are depicted in Figure 5(a).

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