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March 2024

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Lecture
Travelling waves or sequentially activated modules: mapping the granularity of cortical propagation
03/12/2024
11:24

Travelling waves or sequentially activated modules: mapping the granularity of cortical propagation

Dr. Mark Shein-Idelson | Dept of Neurobiology, Faculty of Life Sciences Tel Aviv University

Tue, Mar 12, 12:30 | Gerhard M.J. Schmidt Lecture Hall

: Numerous studies have identified travelling waves in the cortex and suggested they play important roles in brain processing. These waves are most often measured using macroscopic methods that do not allow assessing wave dynamics at the single neuron scale and analyzed using techniques that smear neuronal excitability boundaries. In my talk, I will present a new approach for discriminating travelling waves from modular activation. Using this approach I will show that Calcium dynamics in mouse cortex and spiking activity in turtle cortex are dominated by modular activation rather than by propagating waves. I will then show how sequentially activating two discrete brain areas can appear as travelling waves in EEG simulations and present an analytical model in which modular activation generates wave-like activity with variable directions, velocities, and spatial patterns. I will end by illustrating why a careful distinction between modular and wave excitability profiles across scales will be critical for understanding the nature of cortical computations.
 
Lecture
A brain-computer interface for studying long-term changes of hippocampal neural codes
03/13/2024
11:24

A brain-computer interface for studying long-term changes of hippocampal neural codes

Linor Baliti Turgeman-PhD Thesis Defense | Prof. Yaniv Ziv Lab

Wed, Mar 13, 15:30 | Arthur and Rochelle Belfer Building for Biomedical Research

Brain-computer interfaces (BCI), have important applications both in medicine and as a research tool. Typically, BCIs rely on electrode arrays to capture electrical signals, which are then processed by algorithms to translate neural activity into actions of an external device. However, these electrophysiological techniques are often inadequate for tracking large populations of the same neurons over timescales longer than ~1 day. To address this, we developed calcium imaging-based BCI for freely behaving mice, facilitating continuous recording and analysis of specific neuronal populations over extended periods. This BCI allowed investigating the long-term neuronal coding dynamics in the hippocampus, revealing changes in neuronal population activity both within and across days. I am hopeful that this BCI will advance studies on spatial cognition and long-term memory.
 
 
 
 
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Lecture
Dimensionality bottleneck uncovers simple action selection rules in hunting zebrafish
03/19/2024
11:24

Dimensionality bottleneck uncovers simple action selection rules in hunting zebrafish

Dr. Lilach Avitan | Edmond and Lily Safra Center for Brain Sciences The Hebrew University of Jerusalem

Tue, Mar 19, 12:30 | Gerhard M.J. Schmidt Lecture Hall

Animal movements are complex, high-dimensional, and lead to many different consequences. Thus, efficiently quantifying the behavior and uncovering the underlying representation used by the animal pose a great challenge. Tracking freely behaving zebrafish larvae using a high-speed camera and analyzing their movements, we reveal that zebrafish movements can be described using exactly two parameters. Mapping all possible two-dimensional movement representations, we identified the representation used by the fish. We show that fish do not trivially represent distance and angles as separate parameters, but rather mix them nonlinearly. Moreover, when hunting, this specific nonlinear relation depends on the prey angle and further dictates a particular set of potential movements. These results uncover, for the first time, the underlying action selection principles of hunting behavior, suggesting that behind this seemingly complex behavior there is a simple and low-dimensional process.
 
 
 
 
 
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Lecture
Hippocampal pathology and pathophysiology in the development of temporal lobe epileptogenesis
03/24/2024
11:24

Hippocampal pathology and pathophysiology in the development of temporal lobe epileptogenesis

Prof. Robert S. Sloviter | The Neuroscience Institute MRC 245 Morehouse School of Medicine, Atlanta GA

Sun, Mar 24, 11:00 | Gerhard M.J. Schmidt Lecture Hall

In families with febrile seizures and temporal lobe epilepsy, mutations affecting different GABAergic mechanisms suggest that failure of chloride conductance to limit depolarization may be directly epileptogenic. This “GABAergic disinhibition” hypothesis has been discounted historically for two reasons. First, early attempts to produce hippocampal sclerosis and epilepsy simply by eliminating hippocampal GABA neurons consistently failed to do so. Second, the notion persists that because clinical epilepsy diagnosis is typically delayed for years or decades after brain injury, temporal lobe epileptogenesis should be presumed to involve a complex pathological transformation process that reaches completion during this “latent period.” Recent advances clarify both issues. Although spatially limited hippocampal GABA neuron ablation causes only submaximal granule cell hyperexcitability, more spatially extensive ablation maximizes granule cell hyperexcitability and triggers nonconvulsive granule cell status epilepticus, hippocampal sclerosis, and epilepsy. Recent studies also show that disinhibited granule cells begin to generate clinically subtle seizures immediately post-injury, and these seizures then gradually increase in duration to become clinically obvious. Therefore, rather than being a seizure-free “gestational” state of potentially interruptible epileptogenesis, the “latent period” is more likely an active epileptic state when barriers to seizure spread and clinical expression are gradually overcome by a kindling process. The likelihood that an epileptic brain state exists long before clinical diagnosis has significant implications for anti-epileptogenesis studies. The location, magnitude, and spatial extent of inherited, autoimmune, and injury-induced disinhibition may determine the latency to clinical diagnosis and establish the continuum between the benign, treatable, and refractory forms of temporal lobe epilepsy.
 
 
 
 
 
 
 
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