Neuroscience seminars

For decades dynamical systems theory played a pivotal role in theoretical and computational neuroscience, as it links biophysical and biochemical processes to neural computation. In fact, dynamical systems are computationally universal. Rather than hand-crafting computational theories of neural function based on dynamical systems, recent developments in scientific machine learning (ML) and AI suggest that we may be able to infer such dynamical-computational models directly from neurophysiological and behavioral observations. This is called dynamical systems reconstruction (DSR), the learning of generative surrogate models of the underlying dynamics, including its long-term temporal and geometrical properties, from time series data. In my talk I will cover recent ML/AI architectures, training algorithms, and validation procedures for DSR. I will discuss specifically how recent AI architectures for DSR can integrate neuroscience data from multiple modalities (like multiple single-unit recordings and behavioral choices), across diverse time scales, and across many different animals and task designs, into a joint DSR model. This provides first steps toward dynamical systems based AI foundation models for neuroscience. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2025-04-23. Recording duration: 00:53:24.

Fear learning induces synaptic potentiation between engram neurons in the rat lateral amygdala. This study by Marios Abatis et al. demonstrates how fear conditioning strengthens synaptic connections between engram cells in the lateral amygdala, revealed through optogenetic identification of neuronal ensembles and electrophysiological measurements. The work provides crucial insights into memory formation mechanisms at the synaptic level, with implications for understanding anxiety disorders and developing targeted interventions. Presented by Dr. Kenneth Hayworth, this journal club will explore the paper's methodology linking engram cell reactivation with synaptic plasticity measurements, and discuss implications for memory decoding research.

Facial expressions are inherently dynamic, and our visual system is sensitive to subtle changes in their temporal sequence. However, researchers often use dynamic morphs of photographs—simplified, linear representations of motion—to study the neural correlates of dynamic face perception. To explore the brain's sensitivity to natural facial motion, we constructed a novel dynamic face database using generative neural networks, trained on a verified set of video-recorded emotional expressions. The resulting deepfakes, consciously indistinguishable from videos, enabled us to separate biological motion from photorealistic form. Results showed that conventional dynamic morphs elicit distinct responses in the brain compared to videos and photos, suggesting they violate expectations (n400) and have reduced social salience (late positive potential). This suggests that dynamic morphs misrepresent facial dynamism, resulting in misleading insights about the neural and behavioural correlates of face perception. Deepfakes and videos elicited largely similar neural responses, suggesting they could be used as a proxy for real faces in vision research, where video recordings cannot be experimentally manipulated. And yet, despite being consciously undetectable as fake, deepfakes elicited an expectation violation response in the brain. This points to a neural sensitivity to naturalistic facial motion, beyond conscious awareness. Despite some differences in neural responses, the realism and manipulability of deepfakes make them a valuable asset for research where videos are unfeasible. Using these stimuli, we proposed a novel marker for the conscious perception of naturalistic facial motion – Frontal delta activity – which was elevated for videos and deepfakes, but not for photos or dynamic morphs.

Overview of neurosurgery specialty interplay between neurology, psychiatry and neurosurgery. Discussion on benefits and disadvantages of classifications. Presentation of sub-specialties: trauma, oncology, functional, pediatric, vascular and spine. How does an ordinary day of a neurosurgeon look like; outpatient clinic, emergencies, pre/intra/post operative patient care. An ordinary operation. Myth-busting and practical insights of every day practice. An ordinary operation. Hint for research on clinical problems to be solved. The coming ethical frontiers of neuroprosthetics. In part two we will explore the explanatory gap and its significance. We will review the more than 200 theories of the hard problem of consciousness, from the prevailing to the unconventional. Finally, we are going to reflect on the AI advancements and the claims of LLMs becoming conscious

Over the past decade, neuroscience, cognitive science and computer science (“AI”) converged to create specific, image-computable, deep neural network models intended to appropriately abstract, emulate and explain the mechanisms of primate ventral visual processing, up to its deepest neural level, the inferior temporal cortex (IT). Because these leading neuroscientific emulation models — aka “digital twins” — are fully observable and machine-executable, they offer predictive and potential application power that our field’s prior conceptual models did not. Our team’s ongoing work is aimed at asking if current digital twin models might support non-invasive, beneficial brain modulation. In this talk, I will describe a key result: we demonstrate that we can use a digital twin to design spatial patterns of light energy that, when “added” to the organism’s retinal input in the context of ongoing natural visual processing, results in precise modulation (i.e. rate bias) of the pattern of a population of IT neurons (where any intended modulation pattern is chosen ahead of time by the scientist). Because the IT visual neural populations are known to directly connect to and modulate downstream neural circuits (e.g. amygdala) that may underlie psychological affective states (e.g. mood and anxiety), this novel basic science may unlock a new, non-invasive application avenue of potential future human clinical benefit. This progress and new impact possibilities resulted from convergent brain science and AI engineering efforts in the domain of visual object intelligence. I will motivate this as just one example of what I believe will unlock in other domains of human intelligence as brain scientists and AI engineers collaborate to develop machine-executable models of the underlying mechanisms of those still-mysterious domains. CARL VAN VREESWIJK MEMORIAL LECTURE 2025. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2025-04-09. Recording duration: 00:55:49.

Photoreceptor loss is the primary cause behind vision impairment and blindness in diseases such as retinitis pigmentosa and age-related macular degeneration. However, the death of rods and cones allows retinoids to permeate the inner retina, causing retinal ganglion cells to become spontaneously hyperactive, severely reducing the signal-to-noise ratio, and creating interference in the communication between the surviving retina and the brain. Treatments aimed at blocking or reducing hyperactivity improve vision initiated from surviving photoreceptors and could enhance the signal fidelity generated by vision restoration methodologies.

Join us for the Memory Decoding Journal Club, a collaboration between the Carboncopies Foundation and BPF Aspirational Neuroscience. This month, we're diving into a groundbreaking paper: 'Reconstructing a new hippocampal engram for systems reconsolidation and remote memory updating' by Bo Lei, Bilin Kang, Yuejun Hao, Haoyu Yang, Zihan Zhong, Zihan Zhai, and Yi Zhong from Tsinghua University, Beijing Academy of Artificial Intelligence, IDG/McGovern Institute of Brain Research, and Peking Union Medical College. Dr. Randal Koene will guide us through an engaging discussion on these exciting findings and their implications for neuroscience and memory research.

Unlike traditional monoamine-based antidepressants that require weeks to exert effects, ketamine alleviates depression within hours, though its clinical use is limited by side effects. While ketamine was initially thought to work primarily through NMDA receptor (NMDAR) inhibition, our research reveals a more complex mechanism. We demonstrate that NMDAR inhibition alone cannot explain ketamine's sustained antidepressant effects, as other NMDAR antagonists like MK-801 lack similar efficacy. Instead, the (2R,6R)-hydroxynorketamine (HNK) metabolite appears critical, exhibiting antidepressant effects without ketamine's side effects. Paradoxically, our findings suggest an inverted U-shaped dose-response relationship where excessive NMDAR inhibition may actually impede antidepressant efficacy, while some level of NMDAR activation is necessary. The antidepressant actions of ketamine and (2R,6R)-HNK require AMPA receptor activation, leading to synaptic potentiation and upregulation of AMPA receptor subunits GluA1 and GluA2. Furthermore, NMDAR subunit GluN2A appears necessary and possibly sufficient for these effects. This research establishes NMDAR-GluN2A activation as a common downstream effector for rapid-acting antidepressants, regardless of their initial targets, offering promising directions for developing next-generation antidepressants with improved efficacy and reduced side effects.