Past events

Sleep is critical for the stabilization of memories. This process is thought to be supported by the reactivation of memories, thereby strengthening the neural infrastructure supporting them. Theoretical accounts of this consolidation process focus on the process through which memories are independently strengthened, but in natural settings individual memories never exist in a vacuum. In this talk, I will present a series of studies exploring the extent of memory reactivation during sleep in humans, how interactions between memories impact the consolidation process, and the role of encoding context in memory processing during sleep. The main technique used to explore memory reactivation in these studies is targeted memory reactivation, a behavioral manipulation that can selectively bias consolidation during sleep. The results demonstrate that multiple semantically related memories can be simultaneously consolidated during sleep. Additionally, they show that memory reactivation during sleep may involve contextual reinstatement, thereby impacting multiple contextually linked memories. These data suggest that reactivation during sleep is not limited to single memory items, and can occur at the network or brain-state level. Relatedly, we show that reactivating a suppression state during sleep can be used to selectively weaken memories. Taken together, these results inform our current understanding regarding memory consolidation processes and open new avenues for translatable research to alleviate memory-related symptoms in patients suffering from psychiatric disorders.

The human hippocampus plays a crucial role in episodic memory; the who, what, where memories that define our lives. In the rodent, well-defined anatomy and physiology make the structure an ideal model system; amenable to circuit manipulations and observations designed to test hypotheses concerning how memories are formed and used. Here I will present our recent work in mice which combines anatomical characterization, genetic interventions and in vivo recording to address how noncononical inputs and outputs influence information flow in the hippocampus. I will first introduce our study identifying a novelty signaling hub in the hypothalamus – the supramammillary nucleus (SuM). Unique about this region is that it not only responds broadly to novel stimuli, but segregates and selectively routes different types of information to discrete cortical targets, the dentate gyrus (DG) and CA2 fields of the hippocampus, for the modulation of mnemonic processing. Next, I will describe ongoing work focused on how CA2’s output impacts both local and distal circuits, including our identification and characterization of a novel descending glutamatergic projection from CA2 pyramidal cells to PV+ neurons in the MS that can regulate cholinergic tone and hippocampal memory. Zoom link: https://weizmann.zoom.us/j/95406893197?pwd=REt5L1g3SmprMUhrK3dpUDJVeHlrZz09 Meeting ID: 954 0689 3197 Password: 750421

How do we strengthen memories while we sleep? In this talk, I will first focus on the question of how different sleep signatures (slow oscillations, spindles and ripples) interact and facilitate hippocampal-neocortical information transfer. I will then present recent data on actual memory content being reactivated during sleep – both naturally (endogenously) and experimentally (exogenously). Zoom link: https://weizmann.zoom.us/j/95406893197?pwd=REt5L1g3SmprMUhrK3dpUDJVeHlrZz09 Meeting ID: 954 0689 3197 Password: 750421

In the first part of my talk I will show how complex visual inference tasks can be performed with Deep-Learning, in a totally unsupervised way, by training on a single image -- the test image alone. The strong recurrence of information inside a single natural image provides powerful internal examples which suffice for self-supervision of Deep-Networks, without any prior examples or training data. This new paradigm gives rise to true “Zero-Shot Learning”. I will show the power of this approach to a variety of visual tasks, including super-resolution, image-segmentation, transparent layer separation, image-dehazing, and more. In the second part of my talk I will show how self-supervision can be used for “Mind-Reading” (recovering observed visual information from fMRI brain recordings), when only very few fMRI training examples are available.

As bigger neuroscience datasets are generated with novel observation modalities, so grows the need for computational tools to answer basic questions. What different types of neurons exist in a population? How to sort out neurons from their electric activity? How do neurons process information? I will present statistical, machine learning and information-theoretic tools that address such questions. In particular, I will discuss new solutions to the problem of classifying neuron types using genetic markers, amortizing spike-sorting in modern multi-electrode arrays and disentangling the simultaneous presence of synergy and redundancy in neural information processing circuits.

Neuron-glia interactions are key for proper myelination in the brain and for its functionality. To study neuron-glia interaction roles in brain development we focus on the genetic disorder Williams syndrome (WS). WS is a multisystemic neurodevelopmental disorder caused by a de-novo hemizygous deletion of ~26 genes from chromosome 7q11.23. We previously revealed surprising aberrations in myelination and brain development in a novel mouse model for the hypersociability phenotype associated with WS, as a result of a neuronal deletion of the transcription factor Gtf2i, which is one of the genes deleted in WS. In this talk, I will present our recent findings focused on altered white matter and brain development in WS, and discuss potential molecular and cellular explanations for the neurodevelopmental deficits in WS. Specifically, I will present evidence for mitochondrial dysfunction in neurons, and what are the microglial responses to the resultant myelination deficits. Furthermore, to study the implication of our studies from mouse models on human condition, I will show our new data on the altered epigenome of human frontal cortex tissue from WS compared to controls. Finally, I will present our approaches to develop new therapeutic approaches and will update on our clinical trial focused on ameliorating white matter deficits in WS. Hybrid seminar Zoom link: https://weizmann.zoom.us/j/95406893197?pwd=REt5L1g3SmprMUhrK3dpUDJVeHlrZz09 Meeting ID: 954 0689 3197 Password: 750421

Social interactions are essential for animals to survive, reproduce, raise their young. Over the years, my lab has attempted to decipher the unique characteristics of social recognition: what are the unique cues that trigger distinct social behaviors, what is the nature and identity of social behavior circuits, how is the function of these circuits different in males and females and how are they modulated by the animal physiological status? In this lecture, I will describe our recent progress in understanding how different parts of the brain participate in the positive and negative control of parental behavior in males and females, providing a new framework to understand the regulation of adult-infant interactions in health and disease. I will also describe how new approaches in in situ single cell transcript omics have enabled us to uncover specific hypothalamic cell populations involved in distinct social behaviors. Finally, I will describe our most recent work uncovering how specific brain circuits are able to direct adaptive changes in behavior during sickness episodes in mice. Host: Dr. Takashi Kawashima takashi.kawashima@weizmann.ac.il tel: 2995