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The anatomy of synapses – structural basis of long-term potentiation and synaptic scaling Kristen M. Harris Center for Learning and Memory, Section of Neurobiology, University of Texas at Austin, USA [email protected] This talk will emphasize work dedicated to understanding the role of dendritic spines and synapse structure in learning and memory. Long-term potentiation (LTP) of synaptic efficacy is a model of learning and memory that is well-suited to investigate this process. A clear understanding requires the nanometer resolution of three-dimensional (3D) reconstruction from serial section electron microscopy (ssEM). In this talk, I will review our work with ssEM to discover structural synaptic scaling, where synaptic input redistributes from many small to fewer enlarged spines with enlarged synapses by 2 hr after the induction of LTP. These enlarged spines sequester more core structures, including polyribosomes (involved in local protein synthesis), endosomes (a local source of plasma membrane, channels, and other signaling molecules), and smooth endoplasmic reticulum (an organelle that regulates calcium and receptor trafficking). Remarkably, the summed synaptic surface area per unit length of dendrite remains constant across control and LTP conditions. These findings support the hypothesis that competition for intrinsic dendritic resources regulates the number and size of synapses that a mature dendrite can support. I will also present new findings that show several presynaptic changes occur by 2 hr after the induction of LTP including a parallel loss of small axonal boutons and small dendritic spines; a homogeneous redistribution of presynaptic vesicles among the enlarged synapses; and a decrease in the number of presynaptic vesicles per synapse, suggesting either more presynaptic release or less recycling accompanies the expression of LTP. These findings support a synchrony between pre and postsynaptic elements that coordinates and refines synaptic circuitry to express LTP. Short biography Kristen M. Harris, PhD was born in Fargo, ND, and raised in the twin city of Moorhead, MN – her father, while born American, was of 100% Norwegian heritage from the Bergen area. She earned her BS, summa cum laude in Biology, Chemistry and Math, from the Minnesota State University Moorhead, her MS in Neurobiology at the University of Illinois with William Greenough, and her PhD at Northeastern Ohio Universities College of Medicine with Timothy Teyler – himself a postdoctoral graduate from Per Andersen’s laboratory at the University of Oslo. Harris had the great honor to be a member of an International Committee to examine 6 Ph.D. candidates from Prof. Per Andersen’s laboratory in 1995 (not the least of whom were the Mosers now at Trondheim). Hence, her Norwegian roots are strong. She went on to postdoctoral research at Harvard Medical School and remained there on the faculty for 15 years before moving to Boston University where she co-directed a Program in Neuroscience with Howard Eichenbaum. After 4 years at BU, she was recruited as a Georgia Research Alliance Eminent Scholar to the Medical College of Georgia where she built and directed the Synapses and Cognitive Neuroscience Center for 4 years, before moving to the University of Texas-Austin where she is now Professor and Fellow in the new Center for Learning and Memory. She served on the search committee to recruit Laura Colgin (a postdoctoral fellow from the Moser’s laboratory) to UT. She is the recipient of many awards including the National Institutes of Health Javits Merit Award. Her research is at the forefront of the systematic study of synapse structure, especially as it relates to the maturation of synaptic function and long-term potentiation. Spinal motor networks – excitation moving us forward Ole Kiehn Mammalian Locomotor Laboratory, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden [email protected] Brain functions are generated by activity in dedicated neural circuits. A major challenge to modern neuroscientist is to understand the function and mode of operation of such circuits in the complex mammalian brain. For locomotor behaviors, like walking, motor circuits in the spinal cord itself generate the actual timing and coordination of the rhythmic muscle activity. Excitatory neurotransmission is known to play a critical role in the generation of the locomotor rhythm and the drive in these spinal motor networks. Here, I will present data on the identification of excitatory networks in the mammalian spinal cord and brainstem locomotor networks. Among several classes of excitatory interneurons in the spinal cord, V2a interneurons are marked selectively by the expression of the transcription factor Chx10. Using combined physiological and molecular approaches we have determined the role of V2a interneurons in the locomotor network and shown that the V2a interneurons play little or no role in rhythm-generation but drive commissural interneurons to insure left-right alternation during locomotion. The V2a network is organized in a modular fashion along the cord and using genetic tracing and ablation and we show that the V2a interneurons together with other excitatory neurons control specific molecularly defined groups of commissural interneurons involved in left-right alternation. Using a transgenic mouse line that selectively drive light-sensitive channels in glutamatergic excitatory neurons in the spinal cord and brainstem we show that such neurons in the cord are directly responsible for rhythmgeneration and that glutamatergic neurons in the lower hindbrain serve as command neurons for initiating locomotor activity. Surprisingly motor neurons may also - in addition to their classical transmitter acetylcholine - release glutamate from central synapses and activate locomotor networks. Together our experiments provide insights to the principal mode of operation of a large-scale mammalian motor circuit. Short biography Ole Kiehn is Professor at the Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. He obtained a medical degree in 1985 from University of Copenhagen where he also gained his doctoral degree in neurophysiology in 1990. Kiehn trained as a post-dotoctoral fellow at Cornell University in 198990 where after he returned to University of Copenhagen to established his lab. In 2001 he was recruited to Karolinska Institutet. Kiehn’s work on motor neurons has provided new insights to the role of intrinsic membrane properties to normal motor function as well as their contribution to dysfunctional motor symptoms after spinal cord injury. His work on spinal locomotor circuitries controlling walking in mammals has defined some of the fundamental building blocks of the network, including interneuron circuitries controlling left-right coordination and inhibitory and excitatory interneuron networks engaged in pattern formation. In his work he has combined genetic manipulation with electrophysiological and anatomical techniques needed to understand complex network function in the mammalian brain. Kiehn is on the editorial board for Current Opinion of Neurobiology, Journal of Neurophysiology, and Neural Development among others. His is a member of the Nobel Assembly and his work has been acknowledged by the Schellenberg Prize and an endowed Söderberg’s professorship. Worms reveal how the brain works – functional genomics in C. elegans Cori Bargmann Howard Hughes Medical Institute, The Rockefeller University, New York, USA [email protected] All animals and even unicellular organisms recognize other members of their species and interact with them, suggesting that ancient biological systems are involved in these recognition processes. Innate social behaviors emerge from neuronal circuits that interpret sensory information based on an individual’s own genotype, sex, and experience. Our work centers on genes that regulate social behaviors of C. elegans, a nematode worm with a simple and well-characterized nervous system. A specific neuropeptide receptor has different activity levels in wild-type social strains and solitary strains of C. elegans. Neuropeptides like vasopressin and oxytocin and their receptors are also implicated in mammalian social behaviors, suggesting a common genetic vocabulary for sociality. How do genes and the enviroment interact to generate behavior? In C. elegans, a specialized “social brain” integrates the genetic regulation of social preference with environmental context. The genetic and anatomical hub of the social brain is a neuron called RMG, which connects to many other neurons through gap junction synapses. Sensory input into RMG determines whether the environment is appropriate or inappropriate for aggregation. If the environmental context is correct, RMG alters the animal’s behavioral preferences so that it approaches pheromones released by its companions. Regulation of RMG by the neuropeptide receptor switches animals between social and solitary behavioral modes. Short biography Cornelia Isabella Bargmann is Investigator, Howard Hughes Medical Institute, and Torsten N. Wiesel Professor and Head, Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York. Education and Training. 1977-1981: B.S. with a major in Biochemistry, The University of Georgia, Athens, GA. Undergraduate research with Sidney Kushner. 1981-1987: Ph.D., Massachusetts Institute of Technology, Department of Biology. Doctoral research with Robert A. Weinberg at the MIT Cancer Center and the Whitehead Institute for Biomedical Research. Field of study: Cancer biology. 1987-1991: Postdoctoral research with H. Robert Horvitz at the Howard Hughes Medical Institute, Massachusetts Institute of Technology. Field of study: Genetics. Positions. 1991-2004: Assistant/Associate/Full Professor, The University of California, San Francisco, Department of Anatomy and Department of Biochemistry and Biophysics 1995-present: Investigator, Howard Hughes Medical Institute. 2004-present: Torsten N. Wiesel Professor and Head of Laboratory, The Rockefeller University Honors. 1981: Phi Beta Kappa, First Honor Graduate (Valedictorian). 1981: National Science Foundation Predoctoral Fellow. 1987: Helen Hay Whitney Postdoctoral Fellow. 1990: Lucille P. Markey Scholar. 1992: Searle Scholar. 1997: Takasago Award for Research in Olfaction. 1997: W. Alden Spencer Award for Neuroscience Research, Columbia University. 2000: Faculty Mentorship Award, UCSF Graduate Student Association. 2000: Charles J. Herrick Award, The American Association of Anatomists. 2001: Elected Associate of the Neurosciences Research Program. 2002: Elected Fellow of the American Academy of Arts and Sciences. 2003: Elected to the National Academy of Sciences. 2004: Prize of the Dargut and Milena Kemali Foundation for Basic and Clinical Neuroscience. 2006: Elected Fellow of the American Association for the Advancement of Science. 2009: Richard Lounsbery Award in Biology and Medicine, National Academy of Sciences. Editorial Boards. Neuron (1995-), Genes and Development (1998-), Cell (1999-), Current Biology (1999-), Current Opinion in Neurobiology (2010-) Optogenetics: unlocking mysteries of the brain in health and disease Karl Deisseroth Departments of Bioengineering and Psychiatry, Stanford University, Stanford CA, USA [email protected] The technology of optogenetics has allowed millisecond-precision optical control over activity in defined cell types within freely moving mammals. The approach introduced by Karl Deisseroth in August of 2005 has now been adopted by thousands of scientists around the world. In 2010 optogenetics was named Method-of-the-Year across all fields of science and engineering by the Nature journals, and headlined the Breakthroughs-ofthe-Decade piece in Science. Beyond initial tool discovery, Deisseroth’s team has also developed the enabling in vivo methods (molecular targeting, fibreoptics and solid-state optics), and led the application of optogenetics to obtain fundamental insights into neural circuit dynamics in health and disease states such as anxiety and Parkinsonism. Deisseroth’s talk will briefly review this history and also focus in detail on new optogenetic technologies including the third-generation halorhodopsin (Nature 446, 6339, 2007; Cell:141, 1–12, 2010), which has enabled the first optogenetic loss-of-function behavioral results in freely-moving mammals (complementing their earlier gain-offunction work). This recent set of papers has resulted in identifying a causal role for nucleus accumbens cholinergic neurons in cocaine conditioning (Science 330:1677-81, 2010), and allowed Deisseroth’s team to map out a specific amygdala projection causally involved in anxiety (Nature, in press 2011), the most common of the psychiatric diseases. www.stanford.edu/group/dlab/papers/breakthroughscience2010.pdf www.stanford.edu/group/dlab/papers/deisserothnature2010.pdf www.stanford.edu/group/dlab/papers/moynature2010.pdf Short biography Karl Deisseroth received his bachelor's degree summa cum laude from Harvard in 1992, his PhD from Stanford in 1998, and his MD from Stanford in 2000. He completed postdoctoral training, medical internship, and adult psychiatry residency at Stanford, and he was board-certified by the American Board of Psychiatry and Neurology in 2006. He is a faculty member in the Bioengineering and Psychiatry Departments at Stanford, and in the medical school continues as a practicing psychiatrist, employing medications as well as high-speed (action potential-based) brain stimulation treatments (VNS, TMS and others) in patients. Deisseroth’s development of optogenetics in his bioengineering laboratory has allowed millisecond-precision optical control over activity in defined cell types within freely moving mammals, and his team. He has received numerous prestigious and international awards for this work, including the Lawrence C. Katz Prize from Duke University, the Schuetze Prize from Columbia University, the Society for Neuroscience YIA Award, the Koetser Prize, and the Nakasone Prize from the international HFSP, all for optogenetics. www.stanford.edu/group/dlab/optogenetics/sciam.html www.forbes.com/forbes/2010/0719/opinions-lasers-algae-bioengineering-ideas-opinions.html Brain network activity and cognition – grid cells, sense of space and memory Edvard I. Moser Kavli Institute for Systems Neuroscience, NTNU, Trondheim, Norway; [email protected] This talk will focus on the neural substrate of spatial representation in the entorhinal cortex and hippocampus. A key element of the mammalian spatial map is the entorhinal grid cell. Grid cells fire selectively at regularly spaced positions in the environment such that, for each cell, activity is observed only when the animal is at places that together define a repeating triangular pattern tiling the entire environment covered by the animal. The pattern is reminiscent of an abstract coordinate system defining places by distances and directions independently of the particular features of the environment. The scale of the grid map is topographically organized in that the spacing of the grid increases from the dorsal to the ventral end of medial entorhinal cortex. I will show that the organization of the grid map is likely to be modular and that HCN channels contribute to the determination of grid scale. I will follow up by showing that, at each dorsal-ventral level, grid cells co-localize with head-direction cells and border cells, which also contribute to a dynamically updated metric representation of current location. Based on studies using a virus-mediated approach to selectively express photoresponsive channel proteins in entorhinal cells with projections to the hippocampus, I shall finally present preliminary data suggesting that grid cells, head direction cells and border cells may all provide direct input to environment-specific place-cell maps downstream in memory networks of the hippocampus. Short biography Edvard Moser (born 1962) is the Director of the Kavli Institute for Systems Neuroscience and the Centre for the Biology of Memory at the Norwegian University of Science and Technology (NTNU) in Trondheim. A Professor of Neuroscience at NTNU since 1998, Moser studied mathematics, statistics, psychology and neurobiology at the University of Oslo, where he obtained his PhD with Per Andersen. Moser trained as Postdoc at the University of Edinburgh and at the University College London 1994-6. Together with May-Britt Moser, he has since their group was established at NTNU in 1996 studied how spatial location and spatial memory are computed in the brain. Their most noteworthy contribution is probably the discovery of grid cells in the entorhinal cortex, which points to the entorhinal cortex as a hub for the brain network that makes us find our way. They have shown how a variety of functional cell types in the entorhinal microcircuit contribute to representation of self-location, how the outputs of the circuit are used by memory networks in the hippocampus, and how episodic memories are separated from each other in the early stages of the hippocampal memory storage. Edvard Moser is a member of the Board of Reviewing Editors in Science and co-editor of Current Opinion in Neurobiology. He has won several international prizes (including the Spencer, Koetser, Bettencourt, Fernström, and Louis-Jeantet). Nansen as a scientist Roland Huntford Wolfson College, University of Cambridge [email protected] When Fridtjof Nansen presented his doctoral dissertation on the 28th April 1888, he laid the foundations of modern neuroscience. Nonetheless he has never had his due as a neuroscientist. The explanation lies in the sequel. The same year, Nansen made the first crossing of Greenland, revolutionising modern polar exploration by the use of skis. He did so, or so he said, to relieve "fatigue of the brain" after his scientific research. Be that as it may, he became much more famous for his Greenland exploit. He suffered the fate of the polymath. His trailblazing discoveries in neuroscience were overshadowed by his achievements in other spheres, notably exploring the Arctic, oceanography and, yes, even ski jumping. His contemporaries in neuroscience at least understood his worth. In 1891, When W. Waldeyer coined the term 'Neuron' to express the physiological independence of the nerve unit, he quoted Nansen as one of his authorities. So Nansen, as it were, lies at the heart of a celebrated medical term. In his dissertation, Nansen proposed the independence of the neuron, and made a prediscovery of the synapse. In other words he propounded what came to be called the neuron theory. In 1886, he published an abstract of what was to be his dissertation in an English journal, and then the following year in a German paper. Unknown to Nansen, others were working along the same lines, notably the two Swiss doctors, Wilhelm His and August Forel. Nansen, however, got into print first. Irrespective of publishing priority, he was the first explicitly to formulate the doctrine of the neuron theory, and therefore the foundation of modern neuroscience. The development of microscopy also had a hand in Nansen's breakthrough. He was working just as Zeiss put the first apochromatic microscope on the market. The coincidence played a part in Nansen's priority. Personally, I think that Nansen ought to have received the first Nobel Prize for medicine - but that's another story. In an ironical twist, Ramon y Cajal shared the Nobel Prize for 1906 as the impresario of the neuron theory, although sheer publishing chronology suggests that he may well have borrowed the idea of the neuron from Nansen. I propose to put Nansen's work into the context of the intellectual turbulence of nineteenth century Norway, created by the forces of nationalism and the drive to independence. He worked as an individual and, for historical reasons, free from the domination of academies, bureaucrats, official research councils and other corporate forces. In this connection, I propose to trace the genesis of Nansen's ideas. He owed much to foreign guests at the Bergen Museum, where he was doing his research Unlike the world today Nansen was, as someone once put it, no prisoner of deductive reasoning. As a result, or otherwise, he showed the leap of imagination from which discoveries spring. This is the leitmotiv of what I propose to say. That, and the fact that Nansen was a zoologist, specialising in primitive marine creatures, in the belief that study of simple mechanisms give an insight into complex ones. He was almost certainly the first to apply the Golgi reazione nero method of staining microscopic sections to invertebrates. All this goes to show that Nansen proved that sciences should crossfertilize each other, and that the distinction between zoology and medicine is selfdefeating. Finally, I want to offer my explanation of why a small, sparsely populated country on the outskirts of Europe, produced someone of Nansen's calibre. He was not alone. This still has lessons for us today, in the laboratory and outside. Short biography Read physics (disastrously) at university, but it would be best to draw a discreet veil over my undergraduate career. Subsequently worked for the United Nations in Geneva, Nordic correspondent for The Observer, based in Helsinki and Stockholm, 1960-74. Since then, author by profession, living in Cambridge. I am a senior member of Wolfson College, University of Cambridge, with a special interest in Scandinavian history and literature. I held the Alistair Horne Fellowship at St. Antony's College, Oxford University while doing some of the research for my biography of Nansen. .