Acoustic Trauma Changes the Parvalbumin-Positive Neurons in Rat Auditory Cortex.

Congli Liu,Yina Huang,Jingwu Sun,Bin Luo,Tao Xu,Haitao Wang,Xiaopeng Liu

doi:10.1155/2018/9828070

Abstract

Acoustic trauma is being reported to damage the auditory periphery and central system, and the compromised cortical inhibition is involved in auditory disorders, such as hyperacusis and tinnitus. Parvalbumin-containing neurons (PV neurons), a subset of GABAergic neurons, greatly shape and synchronize neural network activities. However, the change of PV neurons following acoustic trauma remains to be elucidated. The present study investigated how auditory cortical PV neurons change following unilateral 1 hour noise exposure (left ear, one octave band noise centered at 16 kHz, 116 dB SPL). Noise exposure elevated the auditory brainstem response threshold of the exposed ear when examined 7 days later. More detectable PV neurons were observed in both sides of the auditory cortex of noise-exposed rats when compared to control. The detectable PV neurons of the left auditory cortex (ipsilateral to the exposed ear) to noise exposure outnumbered those of the right auditory cortex (contralateral to the exposed ear). Quantification of Western blotted bands revealed higher expression level of PV protein in the left cortex. These findings of more active PV neurons in noise-exposed rats suggested that a compensatory mechanism might be initiated to maintain a stable state of the brain.

Highlights

Acoustic overexposure, aging, and ototoxic drugs could lead to auditory disorders including hearing loss, hyperacusis, and tinnitus [1]
In order to make sure that all the subjects have a normal hearing before noise exposure, the Auditory brainstem evoked responses (ABR) thresholds for clicks were determined
The threshold of noise-exposed ear was significantly elevated when the rats were examined 7 days after noise exposure paradigm (76.88 ± 1.01 dB, p < 0 0001, n = 16, Figure 1(e)), while that of the contralateral ears remained unaffected (18.13 ± 0.77 dB, p > 0 05, n = 16, Figure 1(e)), which indicated that rat model with unilateral hearing loss was successfully established

Summary

Introduction

Acoustic overexposure, aging, and ototoxic drugs could lead to auditory disorders including hearing loss, hyperacusis, and tinnitus [1]. Hearing loss-induced elevation of neuronal activity and synchronization is closely related with impaired inhibition [2,3,4]. Cortical inhibition was contributed by nearly 20% interneurons which balance the excitation exerted by glutamatergic neurons. These GABAergic interneurons targeting different compartments of glutamatergic neurons play critical roles in sculpturing cortical circuits. GABA inhibition powerfully influences the frequency tuning curve and receptive field of auditory cortex neurons, and the impaired inhibition is implicated in many neurological disorders. Noise-induced increase of the excitability of principal neurons of auditory stations is largely documented [5,6,7], and the question is how the inhibitory neurons change in this process

Methods

Results

Conclusion