周强
周强,北京大学深圳研究生院教授、化生学院副院长,为 Neuron、PNAS、Journal of Neuroscience等杂志的审稿人。神经生物学博士,毕业于美国纽约州立大学石溪分校,师从美国科学院院士 Roger Nicoll,蒲慕明教授,英国皇家学会会士 Paul Adams 教授。曾先后在美国西奈山医学院担任神经科助理教授,在 Genentech/Roche(罗氏)从事神经系统药物的早期研发工作。在 Nature、 Science、Cell、Neuron、PNAS 等国际知名期刊上发表过30多篇文章。国际上抑制性神经系统功能与调节领域的领军人物,最先证明神经突触减弱与突触棘萎缩相关;在国际上率先证明突触可塑性是大脑感觉功能改变的生理学基础;并率先将显微成像技术与电生理技术相结合来研究神经突触的可塑性。其研究对于理解神经突触可塑性/功能与其形态学变化紧密相连做出了重大贡献。曾获2001年美国国家健康研究院国家研究服务奖、2006年美国埃里森医学基金会新学者奖, 2013年美国生物精神病学会年会最佳展示奖, 以及2016年科学中国人年度人物奖。自2014年回国加入北京大学深圳研究生院之后,已主持多个项目,包括深圳市孔雀人才项目(老年痴呆症生物学研究及药物研发);深圳市细胞生理学重点实验室的建立。
周强
- 职务:课题组组长,教授
- 电话:+86-755-8168-4985
- 邮箱:zhouqiang@pkusz.edu.cn
- 课题组主页:http://web.pkusz.edu.cn/zhouq/
- 教育背景及工作经历2014-至今 教授,北京大学深圳研究生院化生学院
2009-2013 研究员,美国基因和技术公司
2004-2009 助理教授,美国西乃山医学院
2003-2004 副专家,美国加州大学伯克利分校
2001-2003 博士后,美国加州大学伯克利分校
1998-2000 博士后,美国加州大学旧金山分校
1998 博士,美国纽约州立大学石溪分校,神经生物学1993 硕士,美国匹兹堡大学,生理学1990 学士,清华大学,生物化学 - 奖项及荣誉
荣誉/会员身份
1999-2000 国家健康研究院实习生身份(美国加州大学旧金山分校)
2001-2004 国家健康研究院国家研究服务奖
2006-2009 新学者奖(埃里森医学基金会)
2013 美国生物精神病学会年会最佳展示奖
1994-至今 美国神经科学学会会员
编委
Journal of neurological disorders
International journal of neurological research
SM Journal of Depression Research and Treatment
Journal of Systems and Integrative Neuroscience - 研究兴趣
资深的成品管线项目管理经验,为主要成品管线项目的生物学主管,主要研究方向是神经退化性疾病和精神疾病,也负责这些领域的商业开发与合作。
- 代表性成果1. Zhou Q, Godwin DW, O’Malley DM and Adams PR. Visualization of calcium influx through channels that shape the burst and tonic modes of thalamic relay cells. J. Neurophysiol. 77: 2816-2825, 1997.2. Godwin DW, Che D, O’Malley DM and Zhou Q. Photostimulation with caged neurotransmitters using fiber optic light guides. J. Neurosci. Meth. 73: 91-106, 1997.3. Cox CL, Zhou Q and Sherman SM. Glutamate locally activates dendritic outputs of thalamic interneurons. Nature 394: 478-482, 1998.4. Zhou Q, Petersen CCH and Nicoll RA. Effect of reduced vesicular filling on synaptic transmission. J. Physiology 525 (1):195-206, 2000.5. Zhou Q, Xiao MY and Nicoll RA. Contribution of cytoskeleton to the internalization of AMPA receptors. Proc. Natl. Acad. USA. 98: 1261-1266, 2001.6. Frerking M, Schmitz D, Zhou Q, Johansen J and Nicoll RA. Kainate receptors depress excitatory synaptic transmission at CA3CA1 synapses in the hippocampus via a direct presynaptic action. J. Neurosci. 21: 2958-2966, 2001.7. Xiao MY, Zhou Q and Nicoll RA. Metabotropic glutamate receptor activation causes a rapid redistribution of AMPA receptors. Neuropharmacology 41: 664-671, 2001.8. El-Husseini AE, Schnell E, Dakoji S, Sweeney N, Zhou Q, Prange O, Gauthier-Campbell C, Aguilera-Moreno A, Nicoll RA and Bredt DS. Synaptic strength regulated by palmitate cycling on PSD-95. Cell 108: 849-863, 2002.9. Zhou Q, Tao HW and Poo M-m. Reversal and stabilization of synaptic modifications in a developing visual system. Science 300, 1953-1957, 2003.10. O’Malley DM, Zhou Q and Gahtan E. Probing neural circuits in the Zebrafish: a suite of optical techniques. Methods 30: 49-63, 2003.11. Zhou Q, Homma, K and Poo, M-m. Shrinkage of dendritic spines associated with long-term depression of hippocampal synapses. Neuron 44:749-757, 2004.12. González-Maeso J, Weisstaub NV, Zhou M, Chan P, Ivic L, Ang R, Lira A, Bradley-Moore M, Ge Y, Zhou Q, Sealfon SC, Gingrich JA. Hallucinogens recruit specific cortical 5-HT(2A) receptor–mediated signaling pathways to affect behavior. Neuron 53:439-52, 2007.13. Wang X, Yang Y and Zhou Q. Independent expression of synaptic and morphological plasticity associated with long-term depression. J. Neurosci. 27:12419-29, 2007.14. Yang Y, Wang X, Frerking M and Zhou Q. Spine expansion and stabilization associated with long-term potentiation. J. Neurosci. 28:5740-51, 2008.15. Yang Y, Wang X, Frerking M and Zhou Q. Delivery of AMPA receptors to perisynaptic sites precedes the full expression of long-term potentiation. Proc. Natl. Acad. USA. 105: 11388-11393, 2008.16. Wang X, Bozdagi O, Nikitczuk J, Zhai Z, Q. Zhou* and Huntley GW*. Extracellular proteolysis by matrix metalloproteinase-9 drives dendritic spine enlargement and long-term potentiation coordinately. Proc. Natl. Acad. USA. 105:19520-19525, 2008. * - co-corresponding author17. Sebeo J, Bozdagi O, Dumitriu D, Ge Y, Zhou Q and Benson D. Requirement for protein synthesis at young synapses. J. Neurosci. 29: 9778-93, 2009.18. Yang Y, Wang XB, Zhou Q. Perisynaptic GluR2-lacking AMPA receptors control the reversibility of synaptic and spines modifications. Proc. Natl. Acad. USA. 107: 11999-2004, 2010.19. Bozdagi O, Wang XB, Nikitczuk JS, Anderson TR, Bloss EB, Radice GL, Zhou Q, Benson DL, Huntley GW. Persistence of coordinated long-term potentiation and dendritic spine enlargement at mature hippocampal CA1 synapses requires N-cadherin. J Neurosci. 30: 9984-9, 2010.20. Bozdagi O, Sakurai T, Papapetrou D, Wang X, Dickstein DL, Takahashi N, Kajiwara Y, Yang M, Katz AM,Scattoni ML, Harris MJ, Saxena R, Silverman JL, Crawley JN, Zhou Q, Hof PR, Buxbaum JD. Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication. Mol Autism. 1(1):15, 2010.21. Hanson J, Weber M, Meilandt W, Wu T, Luu T, Deng L, Shamloo M, Sheng M, Scearce-Levie K and Qiang Zhou. GluN2B antagonism affects interneurons and leads to immediate and persistent changes in synaptic plasticity, oscillations, and behavior. Neuropsychopharmacology. 38(7):1221-33, 2013.23. Hanson J, Deng L, Hackos D, Lo JS, Lauffer B, Steiner P and Zhou Q. HDAC2 cell-autonomously suppresses excitatory and enhances inhibitory synaptic functions in hippocampal neurons. J. Neurosci. 33:5924-9, 2013.24. Hanson J, La H, Plise E, Chen Y-H, Ding X, Lowe D, Steiner P, Liu L, Scearce-Levie K and Zhou Q. SAHA enhances synaptic function and plasticity in vitro but lack of brain availability in vivo prevents impacts on cognition. Plos One. 8(7):e69964, 2013.25. Pozniak CD, Sengupta Ghosh A, Gogineni A, Hanson JE, Lee SH, Larson JL, Solanoy H, Bustos D, Li H, Ngu H, Jubb AM, Ayalon G, Wu J, Scearce-Levie K, Zhou Q, Weimer RM, Kirkpatrick DS, Lewcock JW. Dual leucine zipper kinase is required for excitotoxicity-induced neuronal degeneration. J Exp Med. 210:2553-67, 2013.26. Hanson JE, Meilandt WJ, Gogineni A, Reynen P, Herrington J, Weimer RM, Scearce-Levie K, Zhou Q. Chronic GluN2B antagonism disrupts behavior in wild-type mice without protecting against synapse loss or memory impairment in Alzheimer's disease mouse models. J Neurosci.34(24):8277-88, 2014.27. Hanson JE, Pare JF, Deng L, Smith Y, Zhou Q. Altered GluN2B NMDA receptor function and synaptic plasticity during early pathology in the PS2APP mouse model of Alzheimer's disease. Neurobiol Dis.74:254-62, 2015.Review articlesZhou Q and Poo M-m. Reversal and consolidation of activity-induced synaptic modifications. Trends. Neurosci. 27:378-83, 2004.Yang Y and Zhou Q. Spine modifications associated with long-term potentiation. Neuroscientist 15: 464-76, 2009.Wang XB, Zhou Q. Spine remodeling and synaptic modification. Mol Neurobiol. 41: 29-41, 2010.Paoletti P, Bellone C and Zhou Q. NMDA receptor subunit diversity: impact on receptor properties, synaptic plasticity and diseases. Nat. Rev. Neuroscience. 14(6):383-400, 2013.Zhou Q and Sheng M. NMDA receptors in nervous system diseases. Neuropharmacology 74:69-75, 2013.Zhou Q. GluN2B-NMDA receptors in Alzheimer's disease: beyond synapse loss and cell death. Neural Regen Res.9(21):1878-9, 2014.
附件列表
词条内容仅供参考,如果您需要解决具体问题
(尤其在法律、医学等领域),建议您咨询相关领域专业人士。