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Abstract：
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.Significance Statement 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.
摘要：
听觉稳态响应（ASSR）是由40Hz声刺激序列引起的皮层振荡。虽然ASSR已广泛应用于临床测量，潜在的神经机制仍然知之甚少。在这项研究中,我们调查了听觉丘脑皮质通路-内侧膝状体（MGB）的不同阶段的贡献，丘脑网状核（TRN）和听觉皮层（AC）-对两性C57BL/6小鼠40HzASSR的产生和调节。我们发现，与40Hz声音刺激同步的神经反应在AC颗粒层中的GABA能神经元和MGB的腹侧分裂（MGBv）中最为突出，受光遗传学操作的TRN神经元的调节。行为实验证实,破坏TRN活性对小鼠辨别40Hz声音的能力具有不利影响。这些发现揭示了有助于解释临床ASSR检查结果的丘脑皮质机制。意义声明我们的研究有助于阐明听觉稳态反应（ASSR）的产生和调节的丘脑皮层机制，它通常用于临床和神经科学研究，以评估听觉功能的完整性。结合一系列电生理和光遗传学实验，我们证明，皮质ASSR的产生取决于源自MGB腹侧分裂到AC颗粒层中GABA能中间神经元的lemniscal丘脑皮质投射。此外，ASSR的丘脑皮质过程受到TRN神经元活动的严格调控。行为实验证实，TRN的功能障碍会导致小鼠在听觉辨别任务中的行为表现中断。
