Department of Ear Nose and Throat/Head and Neck Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.
School of Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands.
J Neurophysiol. 2021 Feb 1;125(2):661-671. doi: 10.1152/jn.00752.2019. Epub 2021 Jan 6.
The thalamic medial geniculate body (MGB) is uniquely positioned within the neural tinnitus networks. Deep brain stimulation (DBS) of the MGB has been proposed as a possible novel treatment for tinnitus, yet mechanisms remain elusive. The aim of this study was to characterize neurophysiologic hallmarks in the MGB after noise exposure and to assess the neurophysiological effects of electrical stimulation of the MGB. Fourteen male Sprague-Dawley rats were included. Nine subjects were unilaterally exposed to a 16-kHz octave-band noise at 115 dB for 90 min, five received sham exposure. Single units were recorded from the contralateral MGB where spontaneous firing, coefficient of variation, response type, rate-level functions, and thresholds were determined. Local field potentials and electroencephalographical (EEG) recordings were performed before and after high-frequency DBS of the MGB. Thalamocortical synchronization and power were analyzed. In total, 214 single units were identified ( = 145 in noise-exposed group, = 69 in control group). After noise exposure, fast-responding neurons become less responsive or nonresponsive without change to their spontaneous rate, whereas sustained- and suppressed-type neurons exhibit enhanced spontaneous activity without change to their stimulus-driven activity. MGB DBS suppressed thalamocortical synchronization in the β and γ bands, supporting suppression of thalamocortical synchronization as an underlying mechanism of tinnitus suppression by high frequency DBS. These findings contribute to our understanding of the neurophysiologic consequences of noise exposure and the mechanism of potential DBS therapy for tinnitus. Separate functional classes of MGB neurons might have distinct roles in tinnitus pathophysiology. After noise exposure, fast-responding neurons become less responsive or nonresponsive without change to their spontaneous firing, whereas sustained and suppressed neurons exhibit enhanced spontaneous activity without change to their stimulus-driven activity. Furthermore, results suggest desynchronization of thalamocortical β and γ oscillations as a mechanism of tinnitus suppression by MGB DBS.
内侧膝状体的丘脑核（MGB）在神经耳鸣网络中具有独特的位置。深脑刺激（DBS）的 MGB 已被提议作为耳鸣的一种可能的新治疗方法，但机制仍难以捉摸。本研究的目的是描述噪声暴露后 MGB 的神经生理特征，并评估 MGB 电刺激的神经生理效应。纳入 14 只雄性 Sprague-Dawley 大鼠。9 只动物单侧暴露于 115dB 的 16kHz 倍频程噪声中 90min，5 只接受假暴露。从对侧 MGB 记录单个单位，确定自发放电、变异系数、反应类型、率-级函数和阈值。在 MGB 高频 DBS 前后进行局部场电位和脑电图（EEG）记录。分析丘脑皮质同步和功率。总共确定了 214 个单个单位（=噪声暴露组 145 个，对照组 69 个）。噪声暴露后，快速反应神经元的反应性降低或无反应，而自发性无变化，而持续和抑制型神经元的刺激驱动活动无变化，自发性活动增强。MGB DBS 抑制了β和γ频段的丘脑皮质同步，支持高频 DBS 抑制耳鸣的机制是抑制丘脑皮质同步。这些发现有助于我们理解噪声暴露的神经生理后果和潜在 DBS 治疗耳鸣的机制。MGB 神经元的不同功能类可能在耳鸣病理生理学中具有不同的作用。噪声暴露后，快速反应神经元的反应性降低或无反应，而自发性无变化，而持续和抑制型神经元的刺激驱动活动无变化，自发性活动增强。此外，结果表明，MGB DBS 抑制耳鸣的机制是丘脑皮质β和γ振荡的去同步。
