{{item.date}}
{{subItem.title}}
{{subItem.subtitle}}




北京生命科学研究所 National Institute of Biological Sciences, Beijing
高级研究员
曹鹏,北京生命科学研究所高级研究员。2000年本科毕业于北京大学生命科学学院,2005年在中科院生物物理所获得博士学位。博士后期间,师从诺贝尔奖得主Thomas Südhof博士,研究神经元囊泡转运的分子机制。2012年回国担任独立PI,课题组聚焦于本能行为的神经机制研究。近十年的研究工作逐步揭示出大脑感知危险的警报防御系统。作为通讯作者,研究成果发表在Cell (2022)、Science (2015)、Nature Neuroscience (2019, 2022) 和Neuron (2017, 2022)等学术刊物。受到国家杰出青年科学基金(2019)等项目的资助。获得张香桐神经科学青年科学家奖(2023)。
报告题目:
恶心-呕吐反应的神经机制初探
报告摘要:
After ingestion of toxin-contaminated food, the brain initiates a series of defensive responses (e.g., nausea, retching, and vomiting). How the brain detects ingested toxin and coordinates diverse defensive responses remains poorly understood. Here, we developed a mouse-based paradigm to study defensive responses induced by bacterial toxins. Using this paradigm, we identified a set of molecularly defined gut-to-brain and brain circuits that jointly mediate toxin-induced defensive responses. The gut-to-brain circuit consists of a subset of Htr3a+ vagal sensory neurons that transmit toxin-related signals from intestinal enterochromaffin cells to Tac1+ neurons in the dorsal vagal complex (DVC). Tac1+ DVC neurons drive retching-like behavior and conditioned flavor avoidance via divergent projections to the rostral ventral respiratory group and lateral parabrachial nucleus, respectively. Manipulating these circuits also interferes with defensive responses induced by the chemotherapeutic drug doxorubicin. These results suggest that food poisoning and chemotherapy recruit similar circuit modules to initiate defensive responses.
{{subItem.subtitle}}
曹鹏,北京生命科学研究所高级研究员。2000年本科毕业于北京大学生命科学学院,2005年在中科院生物物理所获得博士学位。博士后期间,师从诺贝尔奖得主Thomas Südhof博士,研究神经元囊泡转运的分子机制。2012年回国担任独立PI,课题组聚焦于本能行为的神经机制研究。近十年的研究工作逐步揭示出大脑感知危险的警报防御系统。作为通讯作者,研究成果发表在Cell (2022)、Science (2015)、Nature Neuroscience (2019, 2022) 和Neuron (2017, 2022)等学术刊物。受到国家杰出青年科学基金(2019)等项目的资助。获得张香桐神经科学青年科学家奖(2023)。
报告题目:
恶心-呕吐反应的神经机制初探
报告摘要:
After ingestion of toxin-contaminated food, the brain initiates a series of defensive responses (e.g., nausea, retching, and vomiting). How the brain detects ingested toxin and coordinates diverse defensive responses remains poorly understood. Here, we developed a mouse-based paradigm to study defensive responses induced by bacterial toxins. Using this paradigm, we identified a set of molecularly defined gut-to-brain and brain circuits that jointly mediate toxin-induced defensive responses. The gut-to-brain circuit consists of a subset of Htr3a+ vagal sensory neurons that transmit toxin-related signals from intestinal enterochromaffin cells to Tac1+ neurons in the dorsal vagal complex (DVC). Tac1+ DVC neurons drive retching-like behavior and conditioned flavor avoidance via divergent projections to the rostral ventral respiratory group and lateral parabrachial nucleus, respectively. Manipulating these circuits also interferes with defensive responses induced by the chemotherapeutic drug doxorubicin. These results suggest that food poisoning and chemotherapy recruit similar circuit modules to initiate defensive responses.