Basta Dietmar, Ernest Arne
Department of Otolaryngology at UKB, Free University of Berlin, Warener Strasse 7, 12683 Berlin, Germany.
Neurosci Lett. 2004 Sep 30;368(3):297-302. doi: 10.1016/j.neulet.2004.07.030.
The inferior colliculus (IC) in vivo is reportedly subject to a noise-induced decrease of GABA-related inhibitory synaptic transmission accompanied by an amplitude increase of auditory evoked responses, a widening of tuning curves and a higher neuronal discharge rate at suprathreshold levels. However, other in vivo experiments which demonstrated constant neuronal auditory thresholds or unchanged spontaneous activity in the IC after noise exposure did not confirm those findings. Perhaps this can be the result of complex noise-induced interactions between different central auditory structures. It was, therefore, the aim of the present study to investigate the effects of noise exposure on the spontaneous electrical activity of single neurons in a slice preparation of the isolated mouse IC. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun 10:1). After one week, auditory brainstem response (ABR) recordings and extracellular single-unit recordings from spontaneously active neurons within the IC slice were performed in noise-exposed and in normal hearing control mice. Noise-exposed animals showed a significant ABR threshold shift in the whole tested frequency range and a significant lower neuronal spontaneous activity in all investigated isofrequency laminae compared to controls. In both groups, the firing rate of 80% of IC neurons (approximately) increased significantly during the application of the GABA(A) receptor antagonist Bicucullin (10 microM). The present findings demonstrate a noise-related modulation of spontaneous activity in the IC, which possibly contribute to the generation of noise-induced tinnitus and hearing loss.
据报道，体内下丘（IC）会受到噪声诱导的GABA相关抑制性突触传递减少的影响，同时伴有听觉诱发反应幅度增加、调谐曲线变宽以及在阈上水平时神经元放电率升高。然而，其他体内实验表明，噪声暴露后IC中的神经元听觉阈值恒定或自发活动未改变，并未证实这些发现。这可能是不同中枢听觉结构之间复杂的噪声诱导相互作用的结果。因此，本研究的目的是在分离的小鼠IC脑片制备中研究噪声暴露对单个神经元自发电活动的影响。正常听力的小鼠在21日龄时，在麻醉状态下（氯胺酮/隆朋，10:1）暴露于噪声（中心频率10 kHz，声压级115 dB，持续3小时）。一周后，对噪声暴露小鼠和正常听力对照小鼠进行听觉脑干反应（ABR）记录以及IC脑片内自发活动神经元的细胞外单单位记录。与对照组相比，噪声暴露动物在整个测试频率范围内显示出显著的ABR阈值偏移，并且在所有研究的等频层中神经元自发活动显著降低。在两组中，约80%的IC神经元在应用GABA(A)受体拮抗剂荷包牡丹碱（10 microM）期间放电率显著增加。本研究结果表明IC中存在与噪声相关的自发电活动调节，这可能有助于噪声性耳鸣和听力损失的产生。
