我们观察到属于内侧前额叶皮质的边缘前皮质（PrL） 和边缘下皮质（IL）可被前扣带回皮质（ACC）同时兴奋，参与ACC对晕动病（MS）的易化作用，其中的神经机制不清楚。本项目拟综合运用光/化学遗传学、免疫（电镜）染色以及脑片膜片钳等技术，进行以下研究，以期为全面理解MS发生和调控的神经机制、研发新型抗MS策略奠定理论基础：（1）干扰“ACC-PrL/IL-孤束核”神经通路活动，分析该通路影响MS的规律和特点；（2）采用GAD67-GFP、gad2-cre等遗传修饰动物，选择性标记PrL/IL内GABA能和MS相关神经元，在细胞水平解析神经信号经ACC“流向”PrL/IL内MS相关神经元的纤维联系模式、不同类型GABA能神经元构成的局部环路及其调节MS相关神经元兴奋性的方式；（3）研究PrL/IL 内MS相关神经元对来自ACC和GABA能神经元的兴奋和抑制性信号的加工、整合及其被兴奋的机制。

We observed previously that prelimbic and infralimbic cortices (PrL and IL, respectively), the two important components of medial prefrontal cortex, were simultaneously excited by activation of anterior cingulate cortex (ACC), which mediated the role of ACC in facilitating motion sickness (MS). The mechanisms therein, however, remain unclear. In this project, we propose, utilizing modern neuroscience techniques such as opto-/chemogenetic approaches, immunoelctron microscopy, immunoflurescence, patch clamp and extracellular recording techniques, to carry out the following experiments which, after being performed smoothly and successfully, will provide valuable results of the theorectical basis for fully understanding the neural mechanisms underlying MS development and for developing new anti-MS strategies. The related studies involves (1) investigation into the characteristics of MS development associated with the activities of the pathway, “ACC-PrL/IL-nucleus of solitary tract”, as will be parsed by perturbation of the pathway by using opto-/chemogenetic approaches; (2) unveiling, at the cellular level, neural connections between ACC and MS related neurons in PrL/IL, as well as the local circuits structured by distinct GABAergic neuron types and the signal processing modes employed by these GABA neurons, as will be disclosed through selectively labeling the GABAergic and MS-related neurons in PrL and IL on genetically modified animals such as GAD67-GFP、gad2-cre mice; (3) investigating how the MS-related neurons in PrL/IL are electrically excited and the related cellular mechanisms whereby these MS-related neurons integrate and process the excitatory and inhibitory signals from ACC and local GABAergic neurons, respectively.