Krasnow Institute Lecture Room – Rm 229

The symposium, hosted by the Krasnow Institute for Advanced Study and the Santa Fe Institute, seeks to explore the dynamics of the crisis through the lenses of finance, economics, complex systems, neuroeconomics, and computational social science.  (More details)

In conjunction with the symposium, Michael Mauboussin, Chief Investment Strategist of Legg Mason Capital Management, and author of Think Twice: Harnessing the Power of Counterintuition, will give a public lecture entitled “The Prime Directive, Sharks, and the Wisdom of Crowds.”  The lecture will be held at 7:30pm on Thursday, May 17th in Founders Hall Room 134 at the Arlington Campus.  Public guests should RSVP for this free seminar.  Conference attendees need not RSVP.

Dr. Sakmann was awarded the Nobel Prize in Medicine in 1991 with physicist Erwin Neher, for their discoveries on single channels in cells, enabled by their invention of the patch-clamp technique. This ground-breaking technical achievement made it possible to examine, in real time, the operation of individual ion channel proteins. Ion channels are found in the membranes of virtually all cells and create selective pores across membranes that are vital for electrical signaling. Sakmann and Neher examined a broad range of cellular functions, eventually discovering the role that ion channels play in diseases such as diabetes, cystic fibrosis, several cardiovascular diseases and certain neuromuscular disorders. This technique forged new paths in the study of membrane physiology and the creation of novel therapeutics targeting ion channels. In fact, the Nobel Prize committee credited the two scientists with revolutionizing modern biology.

We are honored to  have Dr. Sakmann speak at our weekly seminar series on May 7th at 4:00pm in the Krasnow Lecture Room.  More Details.

Dr. Sakmann’s research

Neurons in the central nervous system are constantly bombarded by signals emanating from other neurons within a densely interconnected network. Such intraneuronal communication, which occurs at sites of cell-to-cell contact called synapses, is essential for responding appropriately to environmental stimuli, for information processing, and for experience-dependent synaptic modifications (plasticity). However, network activity levels can fluctuate greatly, leading to potential problems – too much stimulation of a neuron can lead to seizure-like activity or neurodegeneration, but not enough interrupts information flow and circuit function. To avoid these extremes of activity, various homeostatic mechanisms strive to maintain the “Goldilocks” optimum level of neuronal output, analogous to temperature regulation by thermostats. How do such feedback mechanisms actually work? Do they exist in all neurons and all synapses? Furthermore, how do homeostatic adjustments occur without disrupting “memory” storage thought to be encoded at neuronal synapses? Some surprising recent studies from our laboratory have found that in the hippocampus, a brain structure important in many forms of learning and memory, homeostatic plasticity occurs largely in a cell type- and synapse-specific fashion. In other words, a computational division of labor appears to exist between independently tunable “homeostatic synapses” that function in neuronal gain control, and putative “information-storing” synapses that are spatially separated and shielded from the effects of homeostatic modifications. These studies shed light on the novel interplay and segregation of different forms of plasticity, which has important implications for circuit function in the adult brain.

Krasnow Institute Lecture Room – Rm 229

15 Years: Giorgio Ascoli & Kim “Avrama” Blackwell
5 Years: Robert Axtell, Julia Berzhanskaya, Christina Bishop, Joey Carls, & Theodore Dumas

It is well-known that when a neuron fires an action potential, sodium and potassium ions cross the neuron’s membrane. This process was described quantitatively by Hodgkin and Huxley in the 1950s. But shouldn’t this flow of ions affect the ion concentrations inside and outside the cell? If so, how would this affect the behavior of the neuron? I will describe recent computational studies that address these questions and raise new ones. Insights from bifurcation theory lead to the identification of a common mechanism that underlies several very different neuronal behaviors which have been seen in many different experimental settings.

Conflict situations, either ongoing as in the case of the Sudan or emergent as in the Arab Spring, are situations in which leaders emerge and beliefs change, sometimes quite radically.  In this talk, a social network approach, that considers who interacts with whom, is used to understand who has power and who are the emergent leaders in these situations of conflict.  This approach is extended, to look at the network of issues and the drift in those issues and persons of power over time and across the regions of interest.  By considering the geo-temporal aspects of the network among individuals we gain a better understanding of the conflict dynamics.

Krasnow Institute Lecture Room – Rm 229 – 4:00pm

Recent advances in network science have greatly increased our understanding of the structure and function of many networked systems, ranging from transportation networks, to social networks, the internet, ecosystems, and biochemical and gene transcription pathways.  Network approaches are also increasingly applied to the brain, at several levels of scale from cells to entire brain systems.  We now know that brain networks exhibit a number of characteristic topological features, including small-world attributes, modularity and hubs.  I will review recent work on how complex brain networks are organized, and how their structural topology constrains and shapes their capacity to process and integrate information.  Particular emphasis will be on the large-scale structure and neural dynamics of the human brain.

Neuronal identity or phenotype is largely determined by the constellation of specific genes that are expressed by the specific cell-type. The magnocellular (MCN) oxytocin (OXT)- and vasopressin (AVP)-synthesizing neurons in the hypothalamus exhibit many physiological differences that distinguish them, but the most prominent feature characterizing these phenotypes is their selective expression of the two neuropeptide genes. A persistent and still unresolved fundamental issue has been to determine what  mechanisms are responsible for the highly selective regulation of the cell-type specific expression of the OXT and AVP genes in the MCNs. Previous attempts that have been made to address this question of cell-type specificity by using bioinformatic and various molecular techniques have met with only limited success. In this talk a novel experimental approach to dissect the cis-regulatory elements in the OXT and AVP genes in vivo will be presented. This method uses Adeno-Associated Viral (AAV) vectors expressing gene promoter deletion constructs and utilizes the enhanced green fluorescent protein (EGFP) as the reporter. The AAV constructs are stereotaxically injected into the rat brain above the supraoptic nuclei containing the MCNs and 2 weeks post-injection the rats are sacrificed and assayed for the neuronal localization of the  EGFP. Using this method it has been possible to identify specific DNA regions in the OXT and AVP gene promoters which are responsible for conferring the cell-type specificity of the OXT and AVP genes’ expression in the MCNs.

Krasnow Institute Lecture Room – Rm 229

Dr. Ascoli’s Nomination

Information on the Outstanding Faculty Awards

University Press Release