Szczepaniak W S, Møller A R
Department of Neurological Surgery, University of Pittsburgh School of Medicine, PA 15213, USA.
Electroencephalogr Clin Neurophysiol. 1996 Mar;100(2):158-64. doi: 10.1016/0013-4694(95)00234-0.
Recent investigations have implicated that the central nervous system has a role in the changes that occur in auditory function following acoustic trauma caused by noise exposure. These investigations indicate that the inferior colliculus may be the primary anatomical location in the ascending auditory pathway where noise-induced neuronal plasticity occurs, thereby resulting in changes in the neuronal processing of auditory information. In the present investigation, we show that the amplitudes of all peaks in the click-evoked response from the external nucleus of the inferior colliculus decrease during a 30 min exposure to a tone (104 dB sound pressure level (SPL) at 4 kHz and 8 kHz). After tone exposure, the amplitudes of two of the peaks of the response from the external nucleus of the inferior colliculus that reflect the input from more caudal structures slowly returned to baseline levels, whereas the amplitudes of the two peaks reflecting neuronal activity in the inferior colliculus increased above baseline levels and remained at the increased levels for at least 90 min following exposure to the tone. We also show that exposure to a 4 kHz tone at 104 dB SPL causes changes in the neuronal processing of tonebursts in the form of changes in the temporal integration function for one of the peaks of the response from the external nucleus of the inferior colliculus that originates in the inferior colliculus. Before tone exposure the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure the amplitude of this peak was independent of the duration of the toneburst stimulus. We interpret these changes as evidence that noise exposure (tone exposure) causes changes in the excitability of the inferior colliculus that are not seen in more caudal structures, and these changes are probably a result of a change in the balance between inhibition and excitation in the inferior colliculus.
最近的研究表明，中枢神经系统在噪声暴露引起的听觉创伤后听觉功能变化中发挥作用。这些研究表明，下丘可能是听觉上行通路中发生噪声诱导神经元可塑性的主要解剖位置，从而导致听觉信息神经元处理的变化。在本研究中，我们发现，在下丘外侧核的短声诱发反应中，所有峰值的幅度在暴露于一个纯音（4 kHz和8 kHz时声压级为104 dB）30分钟期间都会降低。纯音暴露后，下丘外侧核反应中反映来自更尾端结构输入的两个峰值的幅度缓慢恢复到基线水平，而反映下丘神经元活动的两个峰值的幅度则高于基线水平，并在暴露于纯音后至少90分钟内保持在升高水平。我们还发现，暴露于104 dB SPL的4 kHz纯音会导致下丘外侧核反应中一个源于下丘的峰值的时间整合功能发生变化，从而引起纯音脉冲串神经元处理的变化。在纯音暴露前，这个峰值的幅度随刺激持续时间增加而降低，但在纯音暴露后，这个峰值的幅度与纯音脉冲串刺激的持续时间无关。我们将这些变化解释为噪声暴露（纯音暴露）导致下丘兴奋性发生变化，而在更尾端结构中未观察到这种变化，这些变化可能是下丘抑制与兴奋平衡改变的结果。
