报告题目：Mitochondrial Excitation-Transcription Coupling in Neuronal Plasticity and Aging
报 告 人：马 欢 教授
主 持 人：徐佳敏 研究员
报告时间：2023年10月20日上午10：00-11：30
报告地点：脑所一楼会议室
报告人简介：
马欢， 浙江大学求是特聘教授、教育部长江学者、国家卫健委医学神经生物学重点实验室副主任、教育部脑与脑机融合国家前沿科学中心/良渚实验室核心研究员。马欢是国家自然科学基金重点和国际合作项目会评专家组成员，国家自然科学委医学科学部神经精神学科“十四五”发展战略专家组成员，中国神经科学学会突触与神经可塑性分会副主任委员，目前主持国家自然科学基金重点项目2项，作为负责人曾获得国家自然科学基金优秀青年基金项目等基金的支持，多年来聚焦神经可塑性调控的分子机制研究，工作以通讯作者发表在本领域一流杂志如Cell、Neuron、Cell Reports和Nature Communications上，相关工作被F1000 多次给予exceptional最高评价，研究成果写入美国神经科学教科书Principles of Neurobiology，推动了对神经可塑性机制与记忆功能的理解。
报告简介：
The intricate tale of aging casts a spotlight on mitochondrial dysfunction as a fundamental instigator. A pervasive catalyst, this phenomenon is intricately intertwined with the passage of time, orchestrating the gradual decline of cellular vigor. In the symposium, my discourse assumes focus upon the enigmatic mechanisms steering the activity-dependent regulation of mitochondria-encoded genes—an orchestration that assumes pivotal significance in the aging narrative. Our investigations have uncovered an elegant interplay—a symphony of neuronal activity seamlessly guiding the expression of mitochondrial-encoded genes. This interaction, once vigorous and harmonious, undergoes an inexorable ebbing as aging unfolds its chronicle. The process of excitation-transcription coupling, while once robust, languishes with time. This transformation, at its culmination, bestows upon us a formidable dual impact—mitochondrial dysfunction and the encumbrance of impaired neuronal function.
We embark upon a systematic exploration, endeavoring to juxtapose the molecular machinery that underpins the divergence between the transcriptional regulation orchestrated by activity in nuclear-encoded genes through the conduits of membrane ion channels, and the parallel symphony echoing within mitochondrial-encoded genes via the corridors of mitochondrial ion channels. Yet, our quest delves further still. The spotlight turns to the mitochondrial calcium uniporter (MCU), a sentinel molecule finely attuned to neuronal activity's rhythm. It is within this domain that the reins of mitochondrial gene transcription are held, a conductor responding to the clarion call of excitation. It strives to illuminate the very essence of the physiological significance and, conversely, the repercussions of the pathological semblance that underlie this intricate dance—this excitation-transcription coupling—within the exquisite expanse of brain mitochondria. In sum, the stage is set for an intricate exploration—a symposium that converges the realms of mitochondrial dysfunction, activity-dependent orchestration, and neuronal intricacies.
