
教师基本信息
姓名:薛磊
职称:研究员
职务:院长助理
电子邮箱:[email protected]
办公地点:D213
办公电话:021-31246756
研究方向
中枢神经系统突触传递功能和分子细胞机制研究,着重于突触前囊泡胞吐/胞吞循环的动力学调控,神经可塑性以及相关计算机建模。
个人简介
教育经历
- 无码av ,2000-2005,神经生物学,博士 
- 无码av ,1996-2000,遗传学,学士 
研究工作经历
- 无码av ,2012年至今,研究员,博士生导师 
- 美国国立卫生研究院,2010年至2012年,研究科学家 
- 美国国立卫生研究院,2005年至2010年,博士后 
学术兼职
- 中国生物物理学会理事 
- 中国生物物理学会“膜与细胞生物物理”分会理事 
- 上海市非线性科学学会理事 
- Scientific Reports 和 BMC Neuroscience编委 
科研项目
- 主持国家自然基金面上项目, 31971159,31770902,31570833,31370828 
- 主持国家重点研发计划课题, 2016YFA0100802 
- 参与国家高技术研究发展计划(863 计划), 2015AA020512 
- 参与上海市自然科学重大项目, 2019-01-07-00-07-E00041 
获奖情况
- 入选浦江人才计划 
- 上海生物物理学会青年科技英才 
授课情况
- 生理学与神经生物学(无码av 本科荣誉课程) 
- 脑科学概论(非生命科学专业) 
- 脑科学导论(信息学院) 
- 脑科学与类脑系统(类脑方向) 
- 神经生物学(无码av 研究生课程) 
招生专业
神经生物学、生物物理学
代表性论文和论著
- Wu YC, Liu QZ, Guo B, Ye FF, Ge JL, and Xue L. BDNF activates postsynaptic TrkB receptors to induce endocannabinoid release and inhibit presynaptic calcium influx at a calyx-type synapse. (2020). the Journal of Neuroscience. 40:8070-8087. 
- Liu QZ#, Hao M#, Zhou ZY#, Ge JL, Wu YC, Zhao LL, Wu X, Feng Y, Gao H, Li S*, and Xue L*. Propofol reduces synaptic strength by inhibiting sodium and calcium channels at nerve terminals. (2019). Protein & Cell. 2019 Sep;10(9):688-693. 
- Jia B, Wu YC, He D, Guo BH, and Xue L. Dynamics of transitions from anti-phase to multiple in-phase synchronizations in inhibitory coupled bursting neurons. (2018). Nonlinear Dynamics. 93: 1599-1618. //doi.org/10.1007/s11071-018-4279-x. 
- Sun ZC#, Ge JL#, Guo B#, Guo J, Hao M, Wu YC, Lin YA, La T, Yao PT, Mei YA, Feng Y* and Xue L*. Extremely Low Frequency Electromagnetic Fields Facilitate Vesicle Endocytosis by Increasing Presynaptic Calcium Channel Expression at a Central Synapse. (2016). Scientific Reports. Feb 18;6:21774. 
- Guo J#, Ge JL#, Hao M#, Sun ZC#, Wu XS, Zhu JB, Wang W, Yao PT, Lin W and Xue L*. A Three-Pool Model Dissecting Readily Releasable Pool Replenishment at the Calyx of Held. (2015). Scientific Reports, 5:9517. 
- Guo J, Sun ZC, Yao PT, Wang HL and Xue L. A Monte Carlo simulation dissecting quantal release at the calyx of Held. (2015). Front Biosci (Landmark Ed) 20:1079–1091. 
- Xue L#*, Sheng J#, Wu XS, Wu W, Luo FJ, Shin Wonchul, Chiang HC, and Wu LG*. Most vesicles in a central nerve terminal participate in recycling. (2013). Journal of Neuroscience,2013 May 15;33(20):8820-6. 
- Xue L#, Zhang Z#, McNeil B, Luo FJ, Wu XS, Sheng JS and Wu LG*. Voltage-dependent calcium channels at the plasma membrane, but not vesicular channels, couple exocytosis to endocytosis. (2012). Cell reports, 1 (6) : 632-638. 
- Xue L#, McNeil BD, Wu XS, Luo FJ, He L and Wu LG*. A Membrane Pool Retrieved via Endocytosis Overshoot at Nerve Terminals: A Study of Its Retrieval Mechanism and Role. (2012). Journal of Neuroscience, 2012 Mar 7; 2(10):3398-404. 
- Xue L# and Wu LG*. Post-tetanic potentiation is caused by two signaling mechanisms affecting quantal size and quantal content. (2010). Journal of Physiology (Lond.) 4987–4994. 
- He L#, Xue L#, Xu J, McNeil B, Bai L, Melicoff E, Adachi R and Wu LG*. Compound vesicle fusion increases quantal size and potentiates synaptic transmission. (2009). Nature, 459(7243):93-7. 

