Neuroscience seminars

Cardiac vagal motor drive originates in the brainstem's cardiac vagal motor neurons (CVNs). Despite well-established cardioinhibitory functions in health, our understanding of CVNs in disease is limited. There is a clear connection of cardiovascular regulation with metabolic and energy expenditure systems. Using high fat diet as a model, this talk will explore how metabolic dysfunction impacts the regulation of cardiac tissue through robust inhibition of CVNs. Specifically, it will present an often overlooked modality of inhibition, tonic gamma-aminobuytric acid (GABA) A-type neurotransmission using an array of techniques from single cell patch clamp electrophysiology to transgenic in vivo whole animal physiology. It also will highlight a unique interaction with the delta isoform of protein kinase C to facilitate GABA A-type receptor expression.

A major challenge in sensory systems is to understand how neurons extract information from the natural environment. Models derived from their responses to artificial stimuli often have a hard time to generalize and predict responses to natural scenes. However, models directly learned on the responses to natural scenes can be hard to interpret. To address this issue, we have recently developed an approach where we add small perturbations to natural scenes and measure how these perturbations change neuronal responses, to better understand the features extracted by sensory neurons. I will show several applications of this approach in the retina, and how it allowed us to uncover non-linear computations performed by ganglion cells, the retinal output. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2025-03-12. Recording duration: 00:47:06.

How can the hippocampal system transition from episodic one-shot learning to a multi-shot learning regime and what is the utility of the resultant neural representations? This talk will explore the role of the dentate gyrus (DG) anatomy in this context. The canonical DG model suggests it performs pattern separation. More recent experimental results challenge this standard model, suggesting DG function is more complex and also supports the precise binding of objects and events to space and the integration of information across episodes. Very recent studies attribute pattern separation and pattern integration to anatomically distinct parts of the DG (the suprapyramidal blade vs the infrapyramidal blade). We propose a computational model that investigates this distinction. In the model the two processing streams (potentially localized in separate blades) contribute to the storage of distinct episodic memories, and the integration of information across episodes, respectively. The latter forms generalized expectations across episodes, eventually forming a cognitive map. We train the model with two data sets, MNIST and plausible entorhinal cortex inputs. The comparison between the two streams allows for the calculation of a prediction error, which can drive the storage of poorly predicted memories and the forgetting of well-predicted memories. We suggest that differential processing across the DG aids in the iterative construction of spatial cognitive maps to serve the generation of location-dependent expectations, while at the same time preserving episodic memory traces of idiosyncratic events.

Over the past thirty years or so, cognitive neuroscience has made spectacular progress understanding the biological mechanisms of consciousness. Consciousness science, as this field is now sometimes called, was not only inexistent thirty years ago, but its very name seemed like an oxymoron: how can there be a science of consciousness? And yet, despite this scepticism, we are now equipped with a rich set of sophisticated behavioural paradigms, with an impressive array of techniques making it possible to see the brain in action, and with an ever-growing collection of theories and speculations about the putative biological mechanisms through which information processing becomes conscious. This is all good and fine, even promising, but we also seem to have thrown the baby out with the bathwater, or at least to have forgotten it in the crib: consciousness is not just mechanisms, it’s what it feels like. In other words, while we know thousands of informative studies about access-consciousness, we have little in the way of phenomenal consciousness. But that — what it feels like — is truly what “consciousness” is about. Understanding why it feels like something to be me and nothing (panpsychists notwithstanding) for a stone to be a stone is what the field has always been after. However, while it is relatively easy to study access-consciousness through the contrastive approach applied to reports, it is much less clear how to study phenomenology, its structure and its function. Here, I first overview work on what consciousness does (the "how"). Next, I ask what difference feeling things makes and what function phenomenology might play. I argue that subjective experience has intrinsic value and plays a functional role in everything that we do.

Neurotrophins (NGF, BDNF, NT-3) are endogenous growth factors that exert neuroprotective effects by preventing neuronal death and promoting neurogenesis. They act by binding to their respective high-affinity, pro-survival receptors TrkA, TrkB or TrkC, as well as to p75NTR death receptor. While these molecules have been shown to significantly slow or prevent neurodegeneration, their reduced bioavailability and inability to penetrate the blood-brain-barrier limit their use as potential therapeutics. To bypass these limitations, our research team has developed and patented small-sized, lipophilic compounds which selectively resemble neurotrophins’ effects, presenting preferable pharmacological properties and promoting neuroprotection and repair against neurodegeneration. In addition, the combination of these molecules with 3D cultured human neuronal cells, and their targeted delivery in the brain ventricles through soft robotic systems, could offer novel therapeutic approaches against neurodegenerative diseases and brain trauma.

Why do individuals, both humans and animals, exhibit personal biases in two-alternative decision-making tasks, even when no clear reason exists to favor one alternative over another? In this talk, I will explore two competing hypotheses to explain these idiosyncratic biases. The first suggests that such tendencies arise from unique personal experiences, where past associations between actions and feedback influence future choices. The second hypothesis proposes that the bias reflects irreducible microscopic heterogeneities in the dynamics of decision-making networks. I will present experimental data and theoretical findings that support the latter hypothesis, shedding new light on the neural mechanisms behind seemingly irrational preferences. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2025-03-05. Recording duration: 00:50:36.

Vulnerability to distraction varies across the general population and significantly affects one’s capacity to stay focused on and successfully complete the task at hand, whether at school, on the road, or at work. In this talk, I will begin by discussing how distractibility is typically assessed in the literature and introduce our innovative ERP approach to measuring it. Since distractibility is a cardinal symptom of ADHD, I will introduce its most widely used paper-and-pencil screening tool for the general population as external validation. Following that, I will present the Load Theory of Attention and explain how we used perceptual load to test the reliability of our neural marker of distractibility. Finally, I will highlight potential future applications of this marker in clinical and educational settings.

In the brain, while early sensory areas encode and process external inputs rapidly, higher-association areas are endowed with slow dynamics to benefit information accumulation over time. This property raises the question of why diverse timescales are well localized rather than being mixed up across the cortex, despite high connection density and an abundance of feedback loops that support reliable signal propagation. In this talk, we will address this question by analyzing a large-scale network model of the primate cortex, and we identify a novel dynamical regime termed "interference-free propagation". In this regime, the mean components of the synaptic currents to each downstream area are imbalanced to ensure signals to propagate reliably, while the temporally fluctuating components of the synaptic inputs governed by upstream areas' timescales are largely canceled out, leading to the localization of its own timescale in each downstream area. Our result provides new insights into the operational regime of the cortex, leading to the coexistence of hierarchical timescale localization and reliable signal propagation. Presented in the van Vreeswijk Theoretical Neuroscience Seminar series (formerly WWTNS) on 2025-02-26. Recording duration: 00:48:02.

Brain Emulation Challenge workshop will tackle cutting-edge topics such as ground-truthing for validation, leveraging artificial datasets generated from virtual brain tissue, and the transformative potential of virtual brain platforms, such as applied to the forthcoming Brain Emulation Challenge.

Brain Emulation Challenge workshop will tackle cutting-edge topics such as ground-truthing for validation, leveraging artificial datasets generated from virtual brain tissue, and the transformative potential of virtual brain platforms, such as applied to the forthcoming Brain Emulation Challenge.

Brain Emulation Challenge workshop will tackle cutting-edge topics such as ground-truthing for validation, leveraging artificial datasets generated from virtual brain tissue, and the transformative potential of virtual brain platforms, such as applied to the forthcoming Brain Emulation Challenge.