Noise exposure enhances auditory cortex responses related to hyperacusis behavior.

Hyperacusis, a marked intolerance to normal environmental sound, is a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases. It has been suggested that an imbalance of excitation and inhibition in the central auditory system (CAS) may play an important role in hyperacusis. Recent studies found that noise exposure, one of the most common causes of hearing loss and tinnitus, can increase the auditory cortex (AC) response, presumably by increasing the gain of the AC. However, it is not clear whether the increased cortical response will affect sound sensitivity and induce hyperacusis. In this experiment, we studied the effects of noise exposure (narrow band noise, 12 kHz, 120 dB SPL, 1 hour) on the physiological response of the inferior colliculus (IC) and the AC, and the behavioral sound reaction in conscious Sprague Dawley rats. Noise exposure induced a decrease of sound evoked potential in the IC. However, significant increases of AC response including sound evoked potentials and the spike firing rates of AC neurons were recorded right after the noise exposure. These results suggest that noise exposure induces hyperexcitability of AC presumably by increasing the post-synaptic response of AC neurons. The behavioral consequence of the noise exposure on sound perception was measured by the amplitude of the acoustic startle response before and after noise exposure in a separate group of rats. Although noise exposure caused a moderate hearing loss, the acoustic startle amplitude at the super-threshold level was significantly increased. These results suggest that noise exposure can cause exaggerated the sound reaction which may be related with the enhanced responsiveness of the AC neurons. This phenomenon may be related with noise induced hyperacusis.This article is part of a Special Issue entitled: Tinnitus Neuroscience.

Sun W ，Deng A ，Jayaram A ，Gibson B ... -  《-》

Hyperexcitability of inferior colliculus and acoustic startle reflex with age-related hearing loss.

Chronic tinnitus and hyperacusis often develop with age-related hearing loss presumably due to aberrant neural activity in the central auditory system (CAS) induced by cochlear pathologies. However, the full spectrum of physiological changes that occur in the CAS as a result age-related hearing loss are still poorly understood. To address this issue, neurophysiological measures were obtained from the cochlea and the inferior colliculus (IC) of 2, 6 and 12 month old C57BL/6J mice, a mouse model for early age-related hearing loss. Thresholds of the compound action potentials (CAP) in 6 and 12 month old mice were significantly higher than in 2 month old mice. The sound driven and spontaneous firing rates of IC neurons, recorded with 16 channel electrodes, revealed mean IC thresholds of 22.8 ± 6.5 dB (n = 167) at 2 months, 37.9 ± 6.2 dB (n = 132) at 6 months and 47.1 ± 15.3 dB (n = 151) at 12 months of age consistent with the rise in CAP thresholds. The characteristic frequencies (CF) of IC neurons ranged from 3 to 32 kHz in 2 month old mice; the upper CF ranged decreased to 26 kHz and 16 kHz in 6 and 12 month old mice respectively. The percentage of IC neurons with CFs between 8 and 12 kHz increased from 36.5% in 2 month old mice, to 48.8% and 76.2% in 6 and 12 month old mice, respectively, suggesting a downshift of IC CFs due to the high-frequency hearing loss. The average spontaneous firing rate (SFRs) of all recorded neurons in 2 month old mice was 3.2 ± 2.5 Hz (n = 167). For 6 and 12 month old mice, the SFRs of low CF neurons (<8 kHz) was maintained at 3-6 spikes/s; whereas SFRs of IC neurons with CFs > 8 kHz increased to 13.0 ± 15.4 (n = 68) Hz at 6 months of age and then declined to 4.8 ± 7.4 (n = 110) spikes/s at 12 months of age. In addition, sound-evoked activity at suprathreshold levels at 6 months of age was much higher than at 2 and 12 months of age. To evaluate the behavioral consequences of sound evoked hyperactivity in the IC, the amplitude of the acoustic startle reflex was measured at 4, 8 and 16 kHz using narrow band noise bursts. Acoustic startle reflex amplitudes in 6 and 12 month old mice (n = 4) were significantly larger than 2 month old mice (n = 4) at 4 and 8 kHz, but not 16 kHz. The enhanced reflex amplitudes suggest that high-intensity, low-frequency sounds are perceived as louder than normal in 6 and 12 month old mice compared to 2 month olds. The increased spontaneous activity, particularly at 6 months, may be related to tinnitus whereas the increase in sound-evoked activity and startle reflex amplitudes may be related to hyperacusis.

Xiong B ，Alkharabsheh A ，Manohar S ，Chen GD ，Yu N ，Zhao X ，Salvi R ，Sun W ... -  《-》

The immediate effects of acoustic trauma on excitation and inhibition in the inferior colliculus: A Wiener-kernel analysis.

Noise-induced tinnitus and hyperacusis are thought to correspond to a disrupted balance between excitation and inhibition in the central auditory system. Excitation and inhibition are often studied using pure tones; however, these responses do not reveal inhibition within the excitatory pass band. Therefore, we used a Wiener-kernel analysis, complemented with singular value decomposition (SVD), to investigate the immediate effects of acoustic trauma on excitation and inhibition in the inferior colliculus (IC). Neural responses were recorded from the IC of three anesthetized albino guinea pigs before and immediately after a one-hour bilateral exposure to an 11-kHz tone of 124 dB SPL. Neural activity was recorded during the presentation of a 1-h continuous 70 dB SPL Gaussian-noise stimulus. Spike trains were subjected to Wiener-kernel analysis in which the second-order kernel was decomposed into excitatory and inhibitory components using SVD. Hearing thresholds between 3 and 22 kHz were elevated (13-47 dB) immediately after acoustic trauma. The presence and frequency tuning of excitation and inhibition in units with a low characteristic frequency (CF; < 3 kHz) was not affected, inhibition disappeared whereas excitation was not affected in mid-CF units (3 < CF < 11 kHz), and both excitation and inhibition disappeared in high-CF units (CF > 11 kHz). This specific differentiation could not be identified by tone-evoked receptive-field analysis, in which inhibitory responses disappeared in all units, along with excitatory responses in high-CF units. This study is the first to apply Wiener-kernel analysis, complemented with SVD, to study the effects of acoustic trauma on spike trains derived from the IC. With this analysis, a reduction of inhibition and preservation of good response thresholds was shown in mid-CF units immediately after acoustic trauma. These neurons may mediate noise-induced tinnitus and/or hyperacusis. Moreover, an immediate profound high-frequency hearing loss was reflected by reduced evoked firing rates and loss of both excitation and inhibition in high-CF units.

Heeringa AN ，van Dijk P 《-》

Behavioral evidence for possible simultaneous induction of hyperacusis and tinnitus following intense sound exposure.

Chen G ，Lee C ，Sandridge SA ，Butler HM ，Manzoor NF ，Kaltenbach JA ... -  《-》

Prolonged Exposure of CBA/Ca Mice to Moderately Loud Noise Can Cause Cochlear Synaptopathy but Not Tinnitus or Hyperacusis as Assessed With the Acoustic Startle Reflex.

Pienkowski M 《Trends in Hearing》