突发！耶鲁大学著名神经生物学家Ronald Duman院士去世，令人惋惜！
根据公众号：SpeciesX 报道，美国耶鲁大学神经生物学家，国际抑郁症领域权威Ronald Duman （罗纳德-杜曼）于2020年02月02日去世，享年66岁。很多中国学者对他应该不陌生，2019年的中国神经科学大会，他来苏州做了大会的报告。当时，接受第一财经记者采访，他表示：“中国神经科学领域的研究虽然起步晚于欧美，但是近年来发展迅速，取得了很多突破性的成果，未来有望赶超欧美。”
Ronald S. Duman是美国国家医学院院士、著名药理学家、耶鲁大学分子精神病研究所所长。在抑郁症领域，取得了非常重要的研究成果。
学习经历：Duman received his doctorate degree from the University of Texas in Houston and conducted postgraduate work at Yale University before joining the faculty there.
学术成绩：He has written and/or co-authored over 300 original papers, reviews and book chapters, and has presented over 250 invited lectures.
社会兼职：Dr. Duman is also on the editorial board of several prestigious journals and serves as a consultant for a number of biotech and pharmaceutical companies.
获奖：Dr. Duman has received several awards for his work, including the Anna-Monika Prize, Nola Maddox Falcone Prize, Janssen Prize, NIMH MERIT Award, and a NARSAD Distinguished Investigator Award.
Brainnews 团队在去年的年初，有报道过Duman教授的文章：Nature Communications：光遗传学助力解码氯胺酮快速抗抑郁新机制 。
2019年1月15日在Nature Communications上发表题为Optogenetic stimulation of medial prefrontal cortex Drd1 neurons produces rapid and long-lasting antidepressant effects的文章， 发现mPFC脑区Drd1（多巴胺受体1型）型神经元介导快速抗抑郁作用，这对于快速抗抑郁新药的研发具有重要的应用价值。 早在2015年杜曼教授就在PNAS上发表了光激活mPFC脑区神经元后可以产生快速抗抑郁作用，并可持续一段时间。本文在此基础上进一步发现mPFC脑区特异性细胞类型Drd1型神经元参与快速抗抑郁作用。
mPFC脑区中Drd1型神经元参与氯胺酮快速抗抑郁的机制模式图
根据其实验室官网的介绍，研究主要内容如下：
Studies in Dr. Duman's laboratory are focused on identifying the molecular and cellular adaptations that underlie the actions of antidepressant drugs and stress. This includes adaptations of receptors, signal transduction proteins, gene transcription factors, neurotrophic factors, and regulation of synaptic processes and even birth of new neurons (neurogenesis) in the adult brain. Preclinical and clinical studies support the hypothesis that neuronal atrophy and cell loss in response to stress contribute to mood disorders. Conversely, the therapeutic action of antidepressants may occur in part via blocking or reversing these damaging effects of stress. A variety of molecular approaches combined with cellular and behavioral studies are conducted to elucidate the basis of complex behavioral abnormalities.
官网列出的代表作包括（全部与抑郁症有关）：
1 Decreased expression of synapse-related genes and loss of synapses in major depressive disorder. Kang HJ, Voleti B, Hajszan T, Rajkowska G, Stockmeier CA, Licznerski P, Lepack A, Majik MS, Jeong LS, Banasr M, Son H, Duman RS. Decreased expression of synapse-related genes and loss of synapses in major depressive disorder. Nature Medicine 2012, 18:1413-7.
2 mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists. Li N, Lee B, Liu RJ, Banasr M, Dwyer JM, Iwata M, Li XY, Aghajanian G, Duman RS. mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists. Science (New York, N.Y.) 2010, 329:959-64.
3 A negative regulator of MAP kinase causes depressive behavior. Duric V, Banasr M, Licznerski P, Schmidt HD, Stockmeier CA, Simen AA, Newton SS, Duman RS. A negative regulator of MAP kinase causes depressive behavior. Nature Medicine 2010, 16:1328-32.
4 Synaptic dysfunction in depression: potential therapeutic targets. Duman RS, Aghajanian GK. Synaptic dysfunction in depression: potential therapeutic targets. Science (New York, N.Y.) 2012, 338:68-72.
5 REDD1 is essential for stress-induced synaptic loss and depressive behavior. Ota KT, Liu RJ, Voleti B, Maldonado-Aviles JG, Duric V, Iwata M, Dutheil S, Duman C, Boikess S, Lewis DA, Stockmeier CA, DiLeone RJ, Rex C, Aghajanian GK, Duman RS. REDD1 is essential for stress-induced synaptic loss and depressive behavior. Nature Medicine 2014, 20:531-5.
6 Optogenetic stimulation of infralimbic PFC reproduces ketamine's rapid and sustained antidepressant actions. Fuchikami M, Thomas A, Liu R, Wohleb ES, Land BB, DiLeone RJ, Aghajanian GK, Duman RS. Optogenetic stimulation of infralimbic PFC reproduces ketamine's rapid and sustained antidepressant actions. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112:8106-11.
7 Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants. Duman RS, Aghajanian GK, Sanacora G, Krystal JH. Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants. Nature Medicine 2016, 22:238-49.
8 GABA interneurons mediate the rapid antidepressant-like effects of scopolamine. Wohleb ES, Wu M, Gerhard DM, Taylor SR, Picciotto MR, Alreja M, Duman RS. GABA interneurons mediate the rapid antidepressant-like effects of scopolamine. The Journal Of Clinical Investigation 2016, 126:2482-94.
9 Integrating neuroimmune systems in the neurobiology of depression. Wohleb ES, Franklin T, Iwata M, Duman RS. Integrating neuroimmune systems in the neurobiology of depression. Nature Reviews. Neuroscience 2016, 17:497-511.
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