Jean Erik Delanois’s research while affiliated with University of California, San Diego and other places

Artificial neural networks (ANNs) show limited performance with scarce or imbalanced training data and face challenges with continuous learning, such as forgetting previously learned data after new tasks training. In contrast, the human brain can learn continuously and from just a few examples. This research explores the impact of 'sleep', an unsupervised phase incorporating stochastic activation with local Hebbian learning rules, on ANNs trained incrementally with limited and imbalanced datasets, specifically MNIST and Fashion MNIST. We discovered that introducing a sleep phase significantly enhanced accuracy in models trained with limited data. When a few tasks were trained sequentially, sleep replay not only rescued previously learned information that had been catastrophically forgetting following new task training but often enhanced performance in prior tasks, especially those trained with limited data. This study highlights the multifaceted role of sleep replay in augmenting learning efficiency and facilitating continual learning in ANNs.

Slow-wave sleep (SWS), characterized by slow oscillations (SOs, <1Hz) of alternating active and silent states in the thalamocortical network, is a primary brain state during Non-Rapid Eye Movement (NREM) sleep. In the last two decades, the traditional view of SWS as a global and uniform whole-brain state has been challenged by a growing body of evidence indicating that SO can be local and can coexist with wake-like activity. However, the mechanisms by which global and local SOs arise from micro-scale neuronal dynamics and network connectivity remain poorly understood. We developed a multi-scale, biophysically realistic human whole-brain thalamocortical network model capable of transitioning between the awake state and SWS, and we investigated the role of connectivity in the spatio-temporal dynamics of sleep SO. We found that the overall strength and a relative balance between long and short-range synaptic connections determined the network state. Importantly, for a range of synaptic strengths, the model demonstrated complex mixed SO states, where periods of synchronized global slow-wave activity were intermittent with the periods of asynchronous local slow-waves. An increase in the overall synaptic strength led to synchronized global SO, while a decrease in synaptic connectivity produced only local slow-waves that would not propagate beyond local areas. These results were compared to human data to validate probable models of biophysically realistic SO. The model producing mixed states provided the best match to the spatial coherence profile and the functional connectivity estimated from human subjects. These findings shed light on how the spatio-temporal properties of SO emerge from local and global cortical connectivity and provide a framework for further exploring the mechanisms and functions of SWS in health and disease.

The performance of artificial neural networks (ANNs) degrades when training data are limited or imbalanced. In contrast, the human brain can learn quickly from just a few examples. Here, we investigated the role of sleep in improving the performance of ANNs trained with limited data on the MNIST and Fashion MNIST datasets. Sleep was implemented as an unsupervised phase with local Hebbian type learning rules. We found a significant boost in accuracy after the sleep phase for models trained with limited data in the range of 0.5-10% of total MNIST or Fashion MNIST datasets. When more than 10% of the total data was used, sleep alone had a slight negative impact on performance, but this was remedied by fine-tuning on the original data. This study sheds light on a potential synaptic weight dynamics strategy employed by the brain during sleep to enhance memory performance when training data are limited or imbalanced.

Slow-wave sleep (SWS), characterized by slow oscillations (SO, <1Hz) of alternating active and silent states in the thalamocortical network, is a primary brain state during Non-Rapid Eye Movement (NREM) sleep. In the last two decades, the traditional view of SWS as a global and uniform whole-brain state has been challenged by a growing body of evidence indicating that SO can be local and can coexist with wake-like activity. However, the understanding of how global and local SO emerges from micro-scale neuron dynamics and network connectivity remains unclear. We developed a multi-scale, biophysically realistic human whole-brain thalamocortical network model capable of transitioning between the awake state and slow-wave sleep, and we investigated the role of connectivity in the spatio-temporal dynamics of sleep SO. We found that the overall strength and a relative balance between long and short-range synaptic connections determined the network state. Importantly, for a range of synaptic strengths, the model demonstrated complex mixed SO states, where periods of synchronized global slow-wave activity were intermittent with the periods of asynchronous local slow-waves. Increase of the overall synaptic strength led to synchronized global SO, while decrease of synaptic connectivity produced only local slow-waves that would not propagate beyond local area. These results were compared to human data to validate probable models of biophysically realistic SO. The model producing mixed states provided the best match to the spatial coherence profile and the functional connectivity estimated from human subjects. These findings shed light on how the spatio-temporal properties of SO emerge from local and global cortical connectivity and provide a framework for further exploring the mechanisms and functions of SWS in health and disease. Author Summary Slow Wave Sleep (SWS) is a primary brain state displayed during Non-Rapid Eye Movement (NREM) sleep. While previously thought of as homogenous waves of activity that sweep across the entire brain, modern research has suggested a more nuanced pattern of activity that can vary between local and global slow wave activity. However, understanding how these states emerge from small scale neuronal dynamics and network connectivity remains unclear. We developed a biophysically realistic model of the human brain capable of generating SWS-like behavior, and investigated the role of connectivity in the spatio-temporal dynamics of these slow waves. We found that the overall strength and a relative balance between long and short-range synaptic connections determined the network behavior - specifically, models with relatively weaker long-range connectivity resulted in mixed states of global and local slow waves. These results were compared to human data, and we found that models producing mixed states provided the best match to the network behavior and functional connectivity of human subject data. These findings shed light on how the spatio-temporal properties of SWS emerge from local and global cortical connectivity and provide a framework for further exploring the mechanisms and functions of SWS in health and disease.

Artificial neural networks overwrite previously learned tasks when trained sequentially, a phenomenon known as catastrophic forgetting. In contrast, the brain learns continuously, and typically learns best when new training is interleaved with periods of sleep for memory consolidation. Here we used spiking network to study mechanisms behind catastrophic forgetting and the role of sleep in preventing it. The network could be trained to learn a complex foraging task but exhibited catastrophic forgetting when trained sequentially on different tasks. In synaptic weight space, new task training moved the synaptic weight configuration away from the manifold representing old task leading to forgetting. Interleaving new task training with periods of off-line reactivation, mimicking biological sleep, mitigated catastrophic forgetting by constraining the network synaptic weight state to the previously learned manifold, while allowing the weight configuration to converge towards the intersection of the manifolds representing old and new tasks. The study reveals a possible strategy of synaptic weights dynamics the brain applies during sleep to prevent forgetting and optimize learning.

Foreword from the editors. We hosted four keynote speakers: Wolf Singer, Bill Bialek, Danielle Bassett, and Sonja Gruen. They enlightened us about computations in the cerebral cortex, the reduction of high-dimensional data, the emerging field of computational psychiatry, and the significance of spike patterns in motor cortex. From the submissions, we also selected four featured orals as particularly noteworthy. They discussed a new role for cortical oscillations as a tempering mechanism, branch-specific computations in Purkinje cells, low frequency entrainment in processing sign language, and decreasing neural heterogeneity as a unifying sign of epilepsy. An additional 16 submissions were selected for shorter oral presentation in the plenary sessions, touching subjects such a spike and population coding, neural computation and interaction, astrocytic and dopaminergic modulation of plasticity, several kinds of sensory processing, reward learning, respiratory and motor control, neural activity propagation and synchronization, and brain organization in epilepsy and schizophrenia. We were also very pleased by the quality of the 213 presented posters, which drew a strong attendance, and the resulting online interactions between presenters and attendees. The full breadth of computational neuroscience was represented, from theory and method development over data analysis to applications.

Continual learning remains an unsolved problem in artificial neural networks. The brain has evolved mechanisms to prevent catastrophic forgetting of old knowledge during new training. Building upon data suggesting the importance of sleep in learning and memory, we tested a hypothesis that sleep protects old memories from being forgotten after new learning. In the thalamocortical model, training a new memory interfered with previously learned old memories leading to degradation and forgetting of the old memory traces. Simulating sleep after new learning reversed the damage and enhanced old and new memories. We found that when a new memory competed for previously allocated neuronal/synaptic resources, sleep replay changed the synaptic footprint of the old memory to allow overlapping neuronal populations to store multiple memories. Our study predicts that memory storage is dynamic, and sleep enables continual learning by combining consolidation of new memory traces with reconsolidation of old memory traces to minimize interference.

Continual learning remains to be an unsolved problem in artificial neural networks. The brain has evolved mechanisms to prevent catastrophic forgetting of old knowledge during new training. Building upon data suggesting importance of sleep in learning and memory, we tested a hypothesis that sleep protects old memories from forgetting. In the thalamocortical model, training a new memory interfered with previously learned old memories leading to degradation and forgetting of the old memory traces. Simulating sleep immediately after new learning reversed the damage and enhanced all memories. We found that when a new memory competed for previously allocated neuronal/synaptic resources, sleep replay changed the synaptic footprint of the old memory to allow overlapping neuronal populations to store multiple memories. Our study predicts that memory storage is dynamic, and sleep enables continual learning by combining consolidation of new memory traces with reconsolidation of old memory traces to minimize interference.