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Register a new userAstrocytes mediate analogous memory in a multi-layer neuron-astrocytic network
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Modeling the neuronal processes underlying short-term working memory remains the focus of many theoretical studies in neuroscience. Here we propose a mathematical model of spiking neuron network (SNN) demonstrating how a piece of information can be maintained as a robust activity pattern for several seconds then completely disappear if no other stimuli come. Such short-term memory traces are preserved due to the activation of astrocytes accompanying the SNN. The astrocytes exhibit calcium transients at a time scale of seconds. These transients further modulate the efficiency of synaptic transmission and, hence, the firing rate of neighboring neurons at diverse timescales through gliotransmitter release. We show how such transients continuously encode frequencies of neuronal discharges and provide robust short-term storage of analogous information. This kind of short-term memory can keep operative information for seconds, then completely forget it to avoid overlapping with forthcoming patterns. The SNN is inter-connected with the astrocytic layer by local inter-cellular diffusive connections. The astrocytes are activated only when the neighboring neurons fire quite synchronously, e.g. when an information pattern is loaded. For illustration, we took greyscale photos of peoples faces where the grey level encoded the level of applied current stimulating the neurons. The astrocyte feedback modulates (facilitates) synaptic transmission by varying the frequency of neuronal firing. We show how arbitrary patterns can be loaded, then stored for a certain interval of time, and retrieved if the appropriate clue pattern is applied to the input.
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Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neural activity. Because synaptic plasticity is the major candidate mechanism for learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. In particular, a prominent aspect that remains debated is how the plasticity mechanisms, that encompass a broad spectrum of temporal and spatial scales, come to play together in a concerted fashion. Here we review and discuss evidence that pinpoints to a possible non-neuronal, glial candidate for such orchestration: the regulation of synaptic plasticity by astrocytes.
Simulating and imitating the neuronal network of humans or mammals is a popular topic that has been explored for many years in the fields of pattern recognition and computer vision. Inspired by neuronal conduction characteristics in the primary visual cortex of cats, pulse-coupled neural networks (PCNNs) can exhibit synchronous oscillation behavior, which can process digital images without training. However, according to the study of single cells in the cat primary visual cortex, when a neuron is stimulated by an external periodic signal, the interspike-interval (ISI) distributions represent a multimodal distribution. This phenomenon cannot be explained by all PCNN models. By analyzing the working mechanism of the PCNN, we present a novel neuron model of the primary visual cortex consisting of a continuous-coupled neural network (CCNN). Our model inherited the threshold exponential decay and synchronous pulse oscillation property of the original PCNN model, and it can exhibit chaotic behavior consistent with the testing results of cat primary visual cortex neurons. Therefore, our CCNN model is closer to real visual neural networks. For image segmentation tasks, the algorithm based on CCNN model has better performance than the state-of-art of visual cortex neural network model. The strength of our approach is that it helps neurophysiologists further understand how the primary visual cortex works and can be used to quantitatively predict the temporal-spatial behavior of real neural networks. CCNN may also inspire engineers to create brain-inspired deep learning networks for artificial intelligence purposes.
Recent years have witnessed an increasing interest in neuron-glia communication. This interest stems from the realization that glia participates in cognitive functions and information processing and is involved in many brain disorders and neurodegenerative diseases. An important process in neuron-glia communications is astrocyte encoding of synaptic information transfer: the modulation of intracellular calcium dynamics in astrocytes in response to synaptic activity. Here, we derive and investigate a concise mathematical model for glutamate-induced astrocytic intracellular Ca2+ dynamics that captures the essential biochemical features of the regulatory pathway of inositol 1,4,5-trisphosphate (IP3). Starting from the well-known two-state Li-Rinzel model for calcium-induced-calcium release, we incorporate the regulation of the IP3 production and phosphorylation. Doing so we extended it to a three-state model (referred as the G-ChI model), that could account for Ca2+ oscillations triggered by endogenous IP3 metabolism as well as by IP3 production by external glutamate signals. Compared to previous similar models, our three-state models include a more realistic description of the IP3 production and degradation pathways, lumping together their essential nonlinearities within a concise formulation. Using bifurcation analysis and time simulations, we demonstrate the existence of new putative dynamical features. The cross-couplings between IP3 and Ca2+ pathways endows the system with self-consistent oscillator properties and favor mixed frequency-amplitude encoding modes over pure amplitude modulation ones. These and additional results of our model are in general agreement with available experimental data and may have important implications on the role of astrocytes in the synaptic transfer of information.
With the rising societal demand for more information-processing capacity with lower power consumption, alternative architectures inspired by the parallelism and robustness of the human brain have recently emerged as possible solutions. In particular, spiking neural networks (SNNs) offer a bio-realistic approach, relying on pulses analogous to action potentials as units of information. While software encoded networks provide flexibility and precision, they are often computationally expensive. As a result, hardware SNNs based on the spiking dynamics of a device or circuit represent an increasingly appealing direction. Here, we propose to use superconducting nanowires as a platform for the development of an artificial neuron. Building on an architecture first proposed for Josephson junctions, we rely on the intrinsic nonlinearity of two coupled nanowires to generate spiking behavior, and use electrothermal circuit simulations to demonstrate that the nanowire neuron reproduces multiple characteristics of biological neurons. Furthermore, by harnessing the nonlinearity of the superconducting nanowires inductance, we develop a design for a variable inductive synapse capable of both excitatory and inhibitory control. We demonstrate that this synapse design supports direct fanout, a feature that has been difficult to achieve in other superconducting architectures, and that the nanowire neurons nominal energy performance is competitive with that of current technologies.
Working memory (WM) allows information to be stored and manipulated over short time scales. Performance on WM tasks is thought to be supported by the frontoparietal system (FPS), the default mode system (DMS), and interactions between them. Yet little is known about how these systems and their interactions relate to individual differences in WM performance. We address this gap in knowledge using functional MRI data acquired during the performance of a 2-back WM task, as well as diffusion tensor imaging data collected in the same individuals. We show that the strength of functional interactions between the FPS and DMS during task engagement is inversely correlated with WM performance, and that this strength is modulated by the activation of FPS regions but not DMS regions. Next, we use a clustering algorithm to identify two distinct subnetworks of the FPS, and find that these subnetworks display distinguishable patterns of gene expression. Activity in one subnetwork is positively associated with the strength of FPS-DMS functional interactions, while activity in the second subnetwork is negatively associated. Further, the pattern of structural linkages of these subnetworks explains their differential capacity to influence the strength of FPS-DMS functional interactions. To determine whether these observations could provide a mechanistic account of large-scale neural underpinnings of WM, we build a computational model of the system composed of coupled oscillators. Modulating the amplitude of the subnetworks in the model causes the expected change in the strength of FPS-DMS functional interactions, thereby offering support for a mechanism in which subnetwork activity tunes functional interactions. Broadly, our study presents a holistic account of how regional activity, functional interactions, and structural linkages together support individual differences in WM in humans.
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