Neurons and Cognition (q-bio.NC)

Abstract: The precise timing of spikes emitted by neurons plays a crucial role in shaping the response of efferent biological neurons. This temporal dimension of neural activity holds significant importance in understanding information processing in neurobiology, especially for the performance of neuromorphic hardware, such as event-based cameras. Nonetheless, many artificial neural models disregard this critical temporal dimension of neural activity. In this study, we present a model designed to efficiently detect temporal spiking motifs using a layer of spiking neurons equipped with heterogeneous synaptic delays. Our model capitalizes on the diverse synaptic delays present on the dendritic tree, enabling specific arrangements of temporally precise synaptic inputs to synchronize upon reaching the basal dendritic tree. We formalize this process as a time-invariant logistic regression, which can be trained using labeled data. To demonstrate its practical efficacy, we apply the model to naturalistic videos transformed into event streams, simulating the output of the biological retina or event-based cameras. To evaluate the robustness of the model in detecting visual motion, we conduct experiments by selectively pruning weights and demonstrate that the model remains efficient even under significantly reduced workloads. In conclusion, by providing a comprehensive, event-driven computational building block, the incorporation of heterogeneous delays has the potential to greatly improve the performance of future spiking neural network algorithms, particularly in the context of neuromorphic chips.

Abstract: This paper addresses the question of the brain's critical dynamics after an injury such as a stroke. It is hypothesized that the healthy brain operates near a phase transition (critical point), which provides optimal conditions for information transmission and responses to inputs. If structural damage could cause the critical point to disappear and thus make self-organized criticality unachievable, it would offer the theoretical explanation for the post-stroke impairment of brain function. In our contribution, however, we demonstrate using network models of the brain, that the dynamics remain critical even after a stroke. In cases where the average size of the second-largest cluster of active nodes, which is one of the commonly used indicators of criticality, shows an anomalous behavior, it results from the loss of integrity of the network, quantifiable within graph theory, and not from genuine non-critical dynamics. We propose a new simple model of an artificial stroke that explains this anomaly. The proposed interpretation of the results is confirmed by an analysis of real connectomes acquired from post-stroke patients and a control group. The results presented refer to neurobiological data; however, the conclusions reached apply to a broad class of complex systems that admit a critical state.