Seminars

Matthew J. Girgenti discusses how research on individual brain cells and the three-dimensional organization of DNA is changing the biological understanding of post-traumatic stress disorder. The seminar examines how these approaches reveal trauma-associated brain changes and identify possible targets for more effective, personalized treatments. Girgenti is a neuroscientist in Yale School of Medicine’s Department of Psychiatry. Jeffrey Borenstein moderates this Meet the Scientist session. Online via the BBRF Zoom webinar. Tuesday 13 October 2026, 14:00 EDT (America/New_York; UTC−4). Follow Register Today on the organizer’s event page to the event-specific Zoom form. Advance registration is available to researchers, students, healthcare providers, mental-health organizations, patients and family members.

Yun Xia presents macrophage–kidney assembloids that address missing immune and vascular components in stem-cell organoids. Directed differentiation, self-organization, genetic perturbation, xenotransplantation and single-cell analysis reveal immune–epithelial interactions. Macrophages from the same parental cells acquire resident phenotypes; diabetic and polycystic kidney models show context-dependent effects on inflammation, epithelial injury and disease progression. Minoru Takasato addresses kidney organoids’ missing urinary outflow by generating bladder tissue from human pluripotent cells. Stepwise differentiation passes through endoderm, hindgut and cloaca; FGF4 posteriorization and growth-factor screening promote urothelial identity. The resulting sacs contain stratified urothelial cell types, stretch and form a barrier, supporting developmental, disease and future therapeutic studies. Online via Zoom. Tuesday 13 October, 11:00–12:30 SGT (Asia/Singapore). Both talks share this session; individual start times are unspecified. Register through the organizer page. Professional, trainee or student status in stem cells, regenerative medicine or an adjacent field is required; organizer approval and recording restrictions apply.

Tom Nowakowski explains lineage barcoding and single-cell sequencing approaches for reconstructing neural stem-cell family trees and early wiring programs in developing mouse and human brains.

How do humans stabilize an inverted pendulum, and why does a balanced pole eventually fall? Drawing on 25 years of fingertip pole-balancing research, this talk examines neural correction delays: longer poles move more slowly relative to the nervous system’s response time. Delay-differential models can stabilize the upright position, yet skilled people still experience falls. The proposed explanation is microchaos arising from interactions among delay, sensory dead zones and frequency-dependent force encoding. A region of transient falling solutions lies next to stable microchaotic dynamics. Such microchaos is absent in virtual frontal-plane balancing tasks, while models of standing postural sway lack the corresponding transient regime. The comparison suggests that human falls, unlike pole falls, are more plausibly associated with medical events or slips and trips.

Anthony Letai discusses how understanding programmed cell death can guide the selection of cancer treatments. The seminar explains how apoptotic signalling can be measured and how these measurements can identify drugs capable of killing cancer cells. Hybrid: New Research Building Auditorium, Georgetown University Medical Center, Washington, DC, and Zoom. Monday 5 October 2026, 16:30–17:30 EDT (America/New_York; UTC−4). Use the attendance registration form or the event’s Zoom link on the organizer page. Organized by Georgetown’s Distinguished Scientist Seminar Series. Letai is Director of the National Cancer Institute. An in-person reception follows the seminar.

To orchestrate complex behaviors in mammals, the cerebral cortex must continuously transmit its processing results to subcortical regions. While internal cortical processing relies on highly selective sparse codes, these descending cortical output streams employ an enigmatic dense code, characterized by high firing rates and low feature selectivity. This dense population code presents a profound paradox: how can downstream regions extract precise, cognitively relevant signals when most cortical output neurons can be active at any moment? We address this paradox by testing the hypothesis that cortex does not lose information when switching to a dense code. Instead, it utilizes a mechanism for sparse-to-dense coding transformations discovered by my laboratory: thalamocortical synapses target specifically the dendritic initiation zone for calcium action potentials (APs), which enables cortical output neurons to transmit multiple information streams simultaneously via a multiplexed 1-2-3 AP syntax. I will provide first evidence that this remarkable synaptic specificity and coding syntax generalize across long-range pathways. Information coupling via an anatomically and biophysically distinct dendritic nexus may hence be a ubiquitous mechanism for sparse-to-dense coding transformations in cortex. Dissecting these mechanistic origins of cortical output streams is only now possible due to a unique in vivo – in silico approach, perfected over two decades, that my laboratory developed for bridging the gaps between dendritic and population-level computations

Mark Harnett presents work on how synaptic organization, nonlinear dendritic processing, and neuronal activity patterns interact to support computation, flexibility, and learning in the adult mammalian neocortex. The Brain and Cognitive Sciences colloquium is followed by a reception.

MIT Biology Colloquium Series talk by David Bilder (University of California, Berkeley), hosted by Yukiko Yamashita, on invertebrate oncology and the ancient evolutionary origins of tumor-host interactions.

Rani Borbara presents brain-wide recordings from more than 150 freely moving C. elegans to examine how anatomical connectivity becomes functional organization during behavior. Cross-animal models map cell-class conditional dependencies and test how synapses, gap junctions, neuromodulation and shared brain states shape circuit dynamics.

Stanford Neurosciences Seminar Series talk by Emery Brown (Massachusetts Institute of Technology, Neuroscience Statistics Research Lab) on deciphering the dynamics of the unconscious brain under general anesthesia, hosted by the Wu Tsai Neurosciences Institute.

Daphna Shohamy and Ashok Litwin-Kumar bridge experimental and computational neuroscience to explain how the brain assigns significance to memories, how dopamine shapes memory-guided decisions, and how bodily signals influence learning. Isabel Low moderates a public discussion and question session.

Shiv Grewal discusses how chromatin and epigenetic mechanisms establish, maintain, and transmit genome states beyond the DNA sequence itself. This NIH Wednesday Afternoon Lecture Series event is offered in person and through NIH VideoCast.

This English-language webinar examines advances in organoid research, production, and drug discovery. Hideya Sakaguchi covers the developmental-biology origins of neural organoid research and its potential for drug discovery, followed by a keynote from Thomas Mitchell of The Organoid Company and a live question session.

Suhrid Ghosh will present work on how cell mechanics and cytoskeletal dynamics shape the evolution of reproductive structures in Drosophila ovaries. Cross-species morphology, ex-vivo live imaging, perturbations of cortical tension, and newly isolated terminal-filament cells reveal how somatic-cell deformability can alter ovariole architecture and reproductive fitness.

Thesis presentation by Tiffany Zhang, graduate fellow in the Vinogradova Lab at The Rockefeller University, on chemical proteomics approaches revealing post-translational remodeling of endosomal pathways during macrophage activation. Open to the tri-institutional community.

Klemens Rottner (Helmholtz Centre for Infection Research, Braunschweig) presents evidence that profilin acts as a master regulator of actin filament dynamics essential for cell migration and growth, controlling both formin- and Arp2/3 complex-dependent actin assembly pathways.

Large recurrent networks are important models in several fields, including neuroscience, machine learning, physics, and applied mathematics. Yet their dynamics are difficult to study directly, because high-dimensional nonlinear systems can exhibit rich behavior that is hard to summarize in terms of individual trajectories. In this talk, I will discuss an approach that seeks to understand such dynamics through the structure of the network’s equilibria. I will focus on a random balanced network of threshold-linear units that undergoes a transition from a single stable equilibrium to extensive chaos as the disorder strength crosses a critical value. Using a combination of Kac–Rice theory, replica calculations, numerical root-finding, and dynamical mean-field theory, we show that the chaotic regime contains an exponentially large number of equilibria. These equilibria are all saddles, but with only a fractionally small number of unstable directions. Surprisingly, despite the completely random connectivity, the equilibria are not scattered randomly through phase space. Instead, they are strongly correlated and confined to a comparatively small region. The chaotic attractor lies within this same region, suggesting a direct geometric link between the organization of unstable equilibria and the collective structure of the dynamics. This picture helps explain why networks with extensive chaos can nevertheless display dynamics dominated by a relatively small number of collective modes. More broadly, the results suggest that the geometry of equilibria provides a useful complementary perspective to dynamical mean-field theory for understanding high-dimensional neural dynamics. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2026-05-27. Recording duration: 00:46:40.

Traditional work in the study of human reward-based learning involves designing an experimental task---often inspired by Reinforcement Learning (RL) theory---and fits a small set of computational models---often inspired by RL algorithms---to that dataset. For example, researchers often model human behavior on bandit tasks using variants of Q-learning. While this approach has been highly productive, leading to landmark discoveries such as the dopamine reward prediction error hypothesis, it also has limitations. This talk focuses on the lack of generalizability of such models: Even if they closely fit behavior on the original task, models derived from the one-task-one-model paradigm usually predict behavior on other tasks quite poorly. I argue that this lack of generalizability is a fundamental problem for the cognitive sciences: we intuitively expect our models to be robust to superficial task differences, such as variations in the number of choice options, reward probabilities, or the exact kind of non-stationarity. I will propose potential solutions to this problem along two dimensions: the behavioral dataset and the computational model. Regarding computational models, I will introduce work in which we moved beyond the limitations of hand-crafted one-off models by employing flexible, data-driven methods. These methods allowed us to compare classes of models instead of individual model instances, allowing us to cover the space of possible models more exhaustively, and innovate cognitive mechanisms very efficiently. For the behavioral dataset, we move from using single learning tasks to a comprehensive task space that encompasses most existing paradigms in the literature, while closing the gaps between them in a near-continuous fashion. Our results suggest that more general models in conjunction with broader datasets can pave the road toward increasingly general models of human reward-based learning and decision making, and a persistent departure from many aspects of RL theory. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2026-05-20. Recording duration: 00:51:19.

Networks of interconnected neurons display diverse patterns of activity. Relating these patterns to the structure of the network is a central goal of theoretical neuroscience. Classic neural field and rate models have been powerful tools for this purpose due to their analytical tractability. Here, we show that the recently-developed combinatorial threshold-linear network (CTLN) model is a mean-field theory for excitatory-inhibitory Hawkes networks, with clustered connectivity, in an inhibition-stabilized regime. This mapping allows us to leverage powerful analytical results for CTLN networks to predict diverse macroscopic dynamics of clustered Hawkes networks, including metastability between various macroscopic fixed points, limit cycles, and chaotic attractors. We will then examine an extension of this approach to models with nonlinear dendritic dynamics, focusing on dendritic calcium spikes.We uncover a marked point process mean-field theory for these n etworks and use this to examine how somatic vs dendritic-targeting connectivity shapes the mean-field equilibrium phase diagram. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2026-05-13. Recording duration: 00:54:14.

Neural oscillations are often proposed to support brain computation by routing information, organizing cell assemblies, or shaping coding dynamics. Yet these ideas usually assume rhythms that are strong, sustained, and regular, whereas in vivo oscillations are often weak, transient, noisy, and variable in frequency and phase. In this talk, I will argue that such “no-metronome” oscillations are not just noisy fluctuations, but coordinated complex dynamics with functional consequences. Combining analyses of neural activity recordings during actual behavior (mice and non-human-primate LFPs and human EEG) with computational modelling, I will discuss evidence that transient oscillatory events can carry task-relevant information and support flexible communication through spatiotemporally structured relationships across populations, timescales, and frequencies. Together, these results suggest that oscillatory weakness and weirdness are not just imperfections, noise to average-out, but part of the functional repertoire of neural computation Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2026-05-06. Recording duration: 00:40:47.