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预期性声音缓解晕动症的神经机制

The Neural Mechanism of Motion Sickness Alleviation by Anticipatory Sound.

基础研究耳科IF 18.9Q1

文献信息

中文摘要

背景: 晕动症(MS)是对冲突运动信号的常见反应,可引起恶心、头晕、不适和活动减少。声音可以减轻MS,但听觉线索如何影响产生这些症状的脑回路尚不清楚。结果:在此,我们利用雄性小鼠的重复旋转范式显示,短暂的预期性音调可减少MS样反应。我们鉴定内侧前庭核(MVN)——一个平衡信号的脑干中心——中表达Cerebellin-2(Cbln2+)的谷氨酸能神经元是这些反应的关键驱动因素。这些神经元通过两个可分离的输出发挥作用:一个投射到腹外侧中脑导水管周围灰质,促进MS样行为;另一个投射到孤束核,可能通过臂旁核参与恶心相关厌恶。预期性音调线索招募从中央杏仁核到抑制Cbln2+ MVN神经元的抑制性通路。结论:这些发现揭示了听觉预测如何抑制驱动MS的前庭回路。

英文摘要

Motion sickness (MS) is a common response to conflicting motion signals and can cause nausea, dizziness, malaise, and reduced activity. Sound can lessen MS, but how auditory cues influence the brain circuits that generate these symptoms is unclear. Here we show, using a repeated rotation paradigm in male mice, that a brief anticipatory tone reduces MS-like responses. We identify Cerebellin-2-expressing (Cbln2+) glutamatergic neurons in the medial vestibular nuclei (MVN), a brainstem center for balance signals, as key drivers of these responses. These neurons act through two separable outputs: a projection to the ventrolateral periaqueductal gray that promotes MS-like behavior, and a projection to the nucleus of the solitary tract that contributes to nausea-related aversion, likely through the parabrachial nucleus. Anticipatory tone cues recruit an inhibitory pathway from the central amygdala to suppress Cbln2+ MVN neurons. These findings reveal how auditory prediction can dampen vestibular circuits that drive MS.