Department of Physiology, China Medical University, Shenyang 110122, People's Republic of China.
Department of Physiology, China Medical University, Shenyang 110122, People's Republic of China
J Neurosci. 2024 Jan 3;44(1):e1166232023. doi: 10.1523/JNEUROSCI.1166-23.2023.
The auditory steady-state response (ASSR) is a cortical oscillation induced by trains of 40 Hz acoustic stimuli. While the ASSR has been widely used in clinic measurement, the underlying neural mechanism remains poorly understood. In this study, we investigated the contribution of different stages of auditory thalamocortical pathway-medial geniculate body (MGB), thalamic reticular nucleus (TRN), and auditory cortex (AC)-to the generation and regulation of 40 Hz ASSR in C57BL/6 mice of both sexes. We found that the neural response synchronizing to 40 Hz sound stimuli was most prominent in the GABAergic neurons in the granular layer of AC and the ventral division of MGB (MGBv), which were regulated by optogenetic manipulation of TRN neurons. Behavioral experiments confirmed that disrupting TRN activity has a detrimental effect on the ability of mice to discriminate 40 Hz sounds. These findings revealed a thalamocortical mechanism helpful to interpret the results of clinical ASSR examinations. Our study contributes to clarifying the thalamocortical mechanisms underlying the generation and regulation of the auditory steady-state response (ASSR), which is commonly used in both clinical and neuroscience research to assess the integrity of auditory function. Combining a series of electrophysiological and optogenetic experiments, we demonstrate that the generation of cortical ASSR is dependent on the lemniscal thalamocortical projections originating from the ventral division of medial geniculate body to the GABAergic interneurons in the granule layer of the auditory cortex. Furthermore, the thalamocortical process for ASSR is strictly regulated by the activity of thalamic reticular nucleus (TRN) neurons. Behavioral experiments confirmed that dysfunction of TRN would cause a disruption of mice's behavioral performance in the auditory discrimination task.
听觉稳态反应（ASSR）是由 40Hz 声刺激的串引起的皮层振荡。虽然 ASSR 在临床测量中得到了广泛的应用，但其潜在的神经机制仍知之甚少。在这项研究中，我们研究了听觉丘脑皮质通路-内侧膝状体（MGB）、丘脑网状核（TRN）和听觉皮层（AC）的不同阶段对雄性和雌性 C57BL/6 小鼠中 40Hz ASSR 的产生和调节的贡献。我们发现，与 40Hz 声音刺激同步的神经反应在 AC 的颗粒层和 MGB 的腹侧部（MGBv）的 GABA 能神经元中最为突出，这些神经元受 TRN 神经元的光遗传学调节。行为实验证实，破坏 TRN 活动会损害小鼠区分 40Hz 声音的能力。这些发现揭示了一个有助于解释临床 ASSR 检查结果的丘脑皮质机制。我们的研究有助于阐明听觉稳态反应（ASSR）产生和调节的丘脑皮质机制，ASSR 在临床和神经科学研究中常用于评估听觉功能的完整性。通过一系列电生理和光遗传学实验，我们证明了皮质 ASSR 的产生依赖于起源于内侧膝状体腹侧部的投射到听觉皮层颗粒层 GABA 能中间神经元的丘系传入。此外，ASSR 的丘脑皮质过程受到丘脑网状核（TRN）神经元活性的严格调节。行为实验证实，TRN 功能障碍会导致小鼠在听觉辨别任务中的行为表现中断。
