Photobiomodulation using low-level 808 nm diode laser rescues cochlear synaptopathy after acoustic overexposure in rat.

A certain degree of noise can cause hearing problems without a permanent change in the hearing threshold, which is called hidden hearing loss and results from partial loss of auditory synapses. Photobiomodulation (PBM) enhances neural growth and connections in the peripheral nervous systems. In this study, we assessed whether PBM could rescue cochlear synaptopathy after acoustic overexposure in rat. PBM was performed for 7 days after noise exposure. The auditory brainstem responses (ABRs) were acquired before and after noise exposure using a tone and a paired-click stimulus. Auditory response to paired click sound with short time interval was performed to evaluate auditory temporal processing ability. In the result, hearing threshold recovered 2 weeks after noise exposure in both groups. Peak wave 1 amplitude of the ABR and ABR recovery threshold did not recover in the noise only group, whereas it fully recovered in the noise + PBM group. The number of synaptic ribbons was significantly different in the control and noise only groups, while there was no difference between the control and noise + PBM group. These results indicate that PBM rescued peak wave 1 amplitude and maintained the auditory temporal processing ability resulting from a loss of synaptic ribbons after acoustic overexposure.

The Effect of CO(2) and KTP laser on the cat saccule and utricle.

OBJECTIVES/HYPOTHESIS: To assess the potential carbon dioxide (CO(2)) and potassium-titanyl-phosphate (KTP) laser-related trauma to the saccule and utricle in a cat model. STUDY DESIGN: Basic science experiment utilizing cat model. METHODS: Twelve adult male cats were divided into two groups-CO(2) and KTP-to assess the potential saccule and/or utricle trauma with direct discharge of laser energy into the vestibule after the stapes was removed. Both groups were subdivided to assess the effects with acute sacrifice and three-month survival. Bone conduction auditory brain-stem response thresholds were used to monitor auditory function. Clinical observation was used to monitor vestibular function. The temporal bones were harvested, processed, and stained with hematoxylin and eosin (H&E) in all animals with the uninvolved side serving as the control. RESULTS: None of the animals demonstrated changes in bone conduction auditory brain-stem responses. None of the animals in the survival group demonstrated clinical vestibular dysfunction. Saccular and utricular wall rupture was observed in all animals sacrificed acutely. None of the saccular and utricular wall ruptures were of a size and location that could be attributed to laser trauma, and none of the saccular and utricular wall ruptures were associated with neuroepithelial trauma. CONCLUSIONS: There is no evidence of a difference between the CO(2) and KTP laser in potential laser-related trauma. Using bone-conducting auditory brain-stem response threshold and clinical monitoring of vestibular function, there was no evidence of clinical auditory or vestibular dysfunction. The histologic evidence of saccular and utricular wall rupture is more consistent with stapes extraction trauma than laser-related trauma.

Cholinergic modulation incorporated with a tone presentation induces frequency-specific threshold decreases in the auditory cortex of the mouse.

Learning-induced or experience-dependent auditory cortical plasticity has often been characterized by frequency-specificity. Studies have revealed the critical role of the cholinergic basal forebrain and acoustic guidance. Cholinergic facilitation of specific thalamocortical inputs potentially determines such frequency-specificity but this issue requires further clarification. To examine the cholinergic effects on thalamocortical circuitry of specific frequency channels, we recorded the responses of cortical neurons while pairing basal forebrain activation or acetylcholine (ACh) microiontophoresis with tone presentations at 10 dB below the neuronal response threshold. We found that both basal forebrain activation and acetylcholine microiontophoresis paired with a tone induced a significant decrease in response threshold of the recorded cortical neurons to the frequency of the paired tone, and that this threshold decrease could be eliminated by atropine microiontophoresis. Our data suggest that cortical acetylcholine specifically facilitates thalamocortical circuitry tuned to the frequency of a presented tone; it is the first, fundamental step towards frequency-specific cortical plasticity evoked by auditory learning and experience.

Mice expressing constitutively active Gsalpha exhibit stimulus encoding deficits similar to those observed in schizophrenia patients.

People with schizophrenia display sensory encoding deficits across a broad range of electrophysiological and behavioral measures, suggesting fundamental impairments in the ability to transduce the external environment into coherent neural representations. This inability to create basic components of complex stimuli interferes with a high fidelity representation of the world and likely contributes to cognitive deficits. The current study evaluates the effects of constitutive forebrain activation of the G(s)alpha G-protein subunit on auditory threshold and gain using acoustic brainstem responses and cortically generated N40 event-related potentials to assess the role of cyclic AMP signaling in sensory encoding. Additionally, we examine the ability of pharmacological treatments that mimic (amphetamine) or ameliorate (haloperidol) positive symptoms of schizophrenia to test the hypothesis that the encoding deficits observed in G(s)alpha transgenic mice can be normalized with treatment. We find that G(s)alpha transgenic mice have decreased amplitude of cortically generated N40 but normal acoustic brainstem response amplitude, consistent with forebrain transgene expression and a schizophrenia endophenotype. Transgenic mice also display decreased stimulus intensity response (gain) in both acoustic brainstem response and N40, indicating corticofugal influence on regions that lack transgene expression. N40 deficits in transgenic animals were ameliorated with low dose haloperidol and reversed with higher dose, suggesting dopamine D2 receptor-linked Gi activity contributes to the impairment. Consistent with this hypothesis, we recreated the G(s)alpha transgenic deficit in wild type animals using the indirect dopamine agonist amphetamine. This transgenic model of sensory encoding deficits provides a foundation for identifying biochemical contributions to sensory processing impairments associated with schizophrenia.

Enriched acoustic environment after noise trauma abolishes neural signs of tinnitus.

Noise-induced hearing loss induces reorganization of the tonotopic map in cat auditory cortex and increases spontaneous firing rate and neural synchrony. We showed previously that keeping cats after noise trauma in an acoustic environment enriched in high frequencies prevents tonotopic map reorganization. Here, we show the effects of low-frequency and high-frequency enriched acoustic environments on spontaneous firing rate and neural synchrony. Exposed cats placed in the quiet environment and in the low-frequency enriched acoustic environment showed increased spontaneous firing rate and synchrony of firing. In contrast, exposed cats placed in the high-frequency enriched acoustic environment did not show significant differences in spontaneous firing rate or synchrony compared with normal hearing controls. This is interpreted as an absence of putative neural signs of tinnitus.

Low-frequency hearing loss in prenatally stressed rats.

We investigated the possibility that hearing thresholds are altered in prenatally stressed rats raised in a normal auditory environment. Pregnant dams were assigned randomly to prenatally stressed and control groups. Half of the dams were subjected to the mild stressors of handling, exposure to a novel cage and saline injection at random times during lights-on daily. The hearing thresholds of young adult male offspring were assessed by recording auditory-evoked brainstem responses to 0.5, 1, 2, 4, 8, 16, 32 and 64 kHz pure tones. The resultant audiograms showed that prenatally stressed offspring had significantly higher hearing thresholds than control animals at 1, 2 and 4 kHz (t-tests, P<0.05). The threshold shifts caused by prenatal stress averaged 7.7 dB across frequencies. We conclude that prenatal stress causes low-frequency hearing loss, possibly due to increased vulnerability to noise-induced hearing loss, accelerated cochlear degeneration and/or disrupted cochlear development.

Bandwidth determines modulatory effects of centrifugal pathways on cochlear hearing desensitization caused by loud sound.

Centrifugal olivocochlear (OC) pathways modulate cochlear hearing losses induced in cats by loud sounds varying in bandwidth from tones to clicks and noise bands, in a variety of conditions. The general effect, always to reduce hearing damage, can be a net effect resulting from complex interactions between OC subcomponents (crossed and uncrossed OC pathways). The interactions between these subcomponents vary with type of loud sound, suggesting that sound bandwidth may be important in determining how OC pathways modulate loud sound-induced hearing loss. This dependency was examined and here it is reported that OC pathways do not alter cochlear hearing losses caused by loud noise with a 2-kHz-wide bandwidth intermediate between the loud sounds of previous studies. Increasing stimulus bandwidth even slightly more, to use a loud 3.5-kHz-wide bandwidth noise as the damaging sound, once again revealed OC modulation of cochlear hearing loss. The fact that OC pathways do not modulate cochlear hearing losses induced by loud 2-kHz-wide noise was demonstrated in three very different test conditions in which OC pathways modulate hearing losses caused by narrower or broader bandwidth sounds. This confirmed that the absence of centrifugal modulation of hearing loss to this particular sound was a robust phenomenon not related to test condition. The absence of overall centrifugal effects was also true at the level of subcomponent pathways; neither crossed nor uncrossed OC pathways individually modulated cochlear hearing losses to the loud 2-kHz-wide noise. This surprising frequency dependency has general implications for centrifugal modulation of cochlear responses.

Corticofugal feedback for auditory midbrain plasticity elicited by tones and electrical stimulation of basal forebrain in mice.

The auditory cortex (AC) is the major origin of descending auditory projections and is one of the targets of the cholinergic basal forebrain, nucleus basalis (NB). In the big brown bat, cortical activation evokes frequency-specific plasticity in the inferior colliculus and the NB augments this collicular plasticity. To examine whether cortical descending function and NB contributions to collicular plasticity are different between the bat and mouse and to extend the findings in the bat, we induced plasticity in the central nucleus of the mouse inferior colliculus by a tone paired with electrical stimulation of the NB (hereafter referred to as tone-ES(NB)). We show here that tone-ES(NB) shifted collicular best frequencies (BFs) towards the frequency of the tone paired with ES(NB) when collicular BFs were different from tone frequency. The shift in collicular BF was linearly correlated to the difference between collicular BFs and tone frequencies. The changes in collicular BFs after tone-ES(NB) were similar to those found in the big brown bat. Compared with cortical plasticity evoked by tone-ES(NB), the pattern of collicular BF shifts was identical but the shifting range of collicular BFs was narrower. A GABA(A) agonist (muscimol) or a muscarinic acetylcholine receptor antagonist (atropine) applied to the AC completely abolished the collicular plasticity evoked by tone-ES(NB). Therefore, our findings strongly suggest that the AC plays a critical role in experience-dependent auditory plasticity through descending projections.

Electrophysiological and speech perception measures of auditory processing in experienced adult cochlear implant users.

OBJECTIVE: This study determined the relationship between auditory evoked potential measures and speech perception in experienced adult cochlear implant (CI) users and compared the CI evoked potential results to those of a group of age- and sex-matched control subjects. METHODS: CI subjects all used the Nucleus CI-22 implant. Middle latency response (MLR), obligatory cortical potentials (CAEP), mismatch negativity (MMN) and P3a auditory evoked potentials were recorded. Speech perception was evaluated using word and sentence tests. RESULTS: Duration of deafness correlated with speech scores with poor scores reflecting greater years of deafness. Na amplitude correlated negatively with duration of deafness, with small amplitudes reflecting greater duration of deafness. Overall, N1 amplitude was smaller in CI than control subjects. Earlier P2 latencies were associated with shorter durations of deafness and higher speech scores. In general, MMN was absent or degraded in CI subjects with poor speech scores. CONCLUSIONS: Auditory evoked potentials are related to speech perception ability and provide objective evidence of central auditory processing differences across experienced CI users. SIGNIFICANCE: Since auditory evoked potentials relate to CI performance, they may be a useful tool for objectively evaluating the efficacy of speech processing strategies and/or auditory training approaches in both adults and children with cochlear implants.

Degradation of temporal resolution in the auditory midbrain after prolonged deafness is reversed by electrical stimulation of the cochlea.

In an animal model of prelingual deafness, we examined the anatomical and physiological effects of prolonged deafness and chronic electrical stimulation on temporal resolution in the adult central auditory system. Maximum following frequencies (Fmax) and first spike latencies of single neurons responding to electrical pulse trains were evaluated in the inferior colliculus of two groups of neonatally deafened cats after prolonged periods of deafness (>2.5 yr): the first group was implanted with an intracochlear electrode and studied acutely (long-deafened unstimulated, LDU); the second group (LDS) received a chronic implant and several weeks of electrical stimulation (pulse rates > or =300 pps). Acutely deafened and implanted adult cats served as controls. Spiral ganglion cell density in all long-deafened animals was markedly reduced (mean <5.8% of normal). Both long-term deafness and chronic electrical stimulation altered temporal resolution of neurons in the central nucleus (ICC) but not in the external nucleus. Specifically, LDU animals exhibited significantly poorer temporal resolution of ICC neurons (lower Fmax, longer response latencies) as compared with control animals. In contrast, chronic stimulation in LDS animals led to a significant increase in temporal resolution. Changes in temporal resolution after long-term deafness and chronic stimulation occurred broadly across the entire ICC and were not correlated with its tonotopic gradient. These results indicate that chronic electrical stimulation can reverse the degradation in temporal resolution in the auditory midbrain after long-term deafness and suggest the importance of factors other than peripheral pathology on plastic changes in the temporal processing capabilities of the central auditory system.

A sound-evoked vestibulomasseteric reflex in healthy humans.

Averaged responses to loud clicks were recorded in the unrectified and rectified masseter electromyogram (EMG) of 18 healthy subjects. Unilateral clicks (0.1 ms, 3 Hz, 70-100 dB NHL), delivered during a steady masseter contraction, evoked bilateral responses that appeared to consist of 2 components on the basis of threshold, latency, and their appearance in rectified EMG. The lowest threshold response appeared as a p16 wave (onset 11-13 ms) in the unrectified EMG and corresponded with a 10- to 12-ms period of inhibition in the rectified EMG. Higher-intensity clicks recruited an earlier p11 response in the unrectified EMG (onset 7.0-9.2 ms) that sometimes appeared as an initial increase in the rectified EMG before suppression. The amplitude of the p11 wave scaled with background EMG level and was asymmetrically modulated by 30 degrees tilt of the whole body. The threshold of the early p11/n15 wave in masseter was the same as the threshold for click-induced vestibulocollic reflexes. Single motor unit recordings demonstrated that responses in masseters corresponded to a silent period in unit firing that began earlier and lasted longer at 100 dB than at 80 dB. We propose that loud clicks induce 2 partially overlapping short-latency reflexes in masseter muscle EMG: a p11/n15 response, which we suggest is of vestibular origin, and a p16/n21 response, which we suggest is equivalent to the previously described jaw-acoustic reflex.

Duration discrimination in the mouse (Mus musculus).

Detection thresholds for an increment in duration of a 10-kHz pure tone were determined in the NMRI mouse using a Go/NoGo-procedure and the method of constant stimuli. Thresholds for reference durations of 50, 100 and 200 ms were obtained presenting the signals at a fixed level or at a level varying by +/-3 dB. Thresholds were determined using signal-detection theory ( d'=1.0 or d'=1.8) and the criterion of 50% correct responses. For a fixed level, the average Weber fraction Delta T/ T (criterion of d'=1.8) significantly decreased from 1.18 or 1.23 at reference durations of 50 or 100 ms, respectively, to 0.97 at a reference duration of 200 ms. Thresholds were on average reduced by 46.8 or 55.4% for the threshold criteria d'=1 or 50% correct responses, respectively. There was no effect of randomizing the level on the discrimination threshold. Duration discrimination in the NMRI mouse does not follow Weber's law. The results are consistent with a mechanism summing up neural impulses over the duration of the stimulus. The psychoacoustic data are compared with results obtained by Brand et al. (J Acoust Soc Am 51:1291-1223, 2000) on the representation of acoustic signal duration in the mouse inferior colliculus.

Imaging of the guinea pig cochlea following round window gadolinium application.

Precise, non-invasive determination of the aetiology and site of pathology of inner ear disorders is difficult. The aim of this study was to describe an alternative method for inner ear visualization, based on local application of the paramagnetic contrast agent gadolinium. Using a 4.7 T MRI scanner, high contrast images of all four cochlear turns were obtained 3.5 h after placing gadolinium on the round window membrane. Gadolinium cleared from the cochlea within 96 h. Auditory brainstem response measurements performed on a separate group of animals showed no significant threshold shifts after the application, indicating that gadolinium is non-toxic to the guinea pig cochlea.

Ultrasonic singing by the blue-throated hummingbird: a comparison between production and perception.

Blue-throated hummingbirds produce elaborate songs extending into the ultrasonic frequency range, up to 30 kHz. Ultrasonic song elements include harmonics and extensions of audible notes, non-harmonic components of audible syllables, and sounds produced at frequencies above 20 kHz without corresponding hearing range sound. To determine whether ultrasonic song elements function in intraspecific communication, we tested the hearing range of male and female blue-throated hummingbirds. We measured auditory thresholds for tone pips ranging from 1 kHz to 50 kHz using auditory brainstem responses. Neither male nor female blue-throated hummingbirds appear to be able to hear above 7 kHz. No auditory brainstem responses could be detected between 8 and 50 kHz at 90 dB. This high-frequency cutoff is well within the range reported for other species of birds. These results suggest that high-frequency song elements are not used in intraspecific communication. We propose that the restricted hummingbird hearing range may exemplify a phylogenetic constraint.

Evaluation of hearing and auditory nerve function by combining ABR, DPOAE and eABR tests into a single recording session.

In this article, we describe an efficient method for testing both auditory receptor and auditory nerve function in a single recording session. Auditory receptor function is tested in response to pure tone, tone burst and click acoustic stimuli (i.e. distortion products of otoacoustic emissions, DPOAE; and auditory-evoked brainstem responses, ABR). The function of the auditory neurons and nerve is measured in response to direct electric current stimulation (i.e. electrically evoked auditory brainstem responses, eABR). All measurements were obtained from anesthetized laboratory rats during single recording sessions using hardware and software stimulation and analysis programs developed by Intelligent Hearing Systems, Miami, FL.

[Soft laser therapy in combination with tebonin i.v. in tinnitus]. / Softlasertherapie in Kombination mit Tebonin i.v. bei Tinnitus.

28 patients were treated with soft-laser therapy. Two-thirds of them had suffered from tinnitus for more than six months and had undergone different therapies before. Each patient was treated twelve times, treatment lasting ten minutes. Before therapy six ml of Tebonin were given i.v. Four minutes later, the laser was positioned at a distance of one centimetre from the patients' mastoid. The laser beam was directed two fingers above the mastoid tip aiming at the lateral wall of the contralateral orbit. Before and three weeks after treatment each patient underwent pure tone audiometry and determination of the tinnitus intensity. Patients were asked to score symptoms before and three weeks after therapy. Hearing levels before and after soft-laser therapy did not show any statistic difference. Three weeks after the last treatment, twenty patients denied any change in tinnitus. Two patients felt an improvement of tinnitus and one patient had recovered completely. Five patients remained undecided about the outcome of therapy. To sum up, according to our results, the trial so far failed to show clear benefits of soft-laser therapy for patients suffering from chronic tinnitus.