Neuron-astrocyte Network Research Articles

Deep Artificial Neural Networks and Neuromorphic Chips for Big Data Analysis: Pharmaceutical and Bioinformatics Applications.

Over the past decade, Deep Artificial Neural Networks (DNNs) have become the state-of-the-art algorithms in Machine Learning (ML), speech recognition, computer vision, natural language processing and many other tasks. This was made possible by the advancement in Big Data, Deep Learning (DL) and drastically increased chip processing abilities, especially general-purpose graphical processing units (GPGPUs). All this has created a growing interest in making the most of the potential offered by DNNs in almost every field. An overview of the main architectures of DNNs, and their usefulness in Pharmacology and Bioinformatics are presented in this work. The featured applications are: drug design, virtual screening (VS), Quantitative Structure–Activity Relationship (QSAR) research, protein structure prediction and genomics (and other omics) data mining. The future need of neuromorphic hardware for DNNs is also discussed, and the two most advanced chips are reviewed: IBM TrueNorth and SpiNNaker. In addition, this review points out the importance of considering not only neurons, as DNNs and neuromorphic chips should also include glial cells, given the proven importance of astrocytes, a type of glial cell which contributes to information processing in the brain. The Deep Artificial Neuron–Astrocyte Networks (DANAN) could overcome the difficulties in architecture design, learning process and scalability of the current ML methods.

Neuroprotective Role of Gap Junctions in a Neuron Astrocyte Network Model

A detailed biophysical model for a neuron/astrocyte network is developed to explore mechanisms responsible for the initiation and propagation of cortical spreading depolarizations and the role of astrocytes in maintaining ion homeostasis, thereby preventing these pathological waves. Simulations of the model illustrate how properties of spreading depolarizations, such as wave speed and duration of depolarization, depend on several factors, including the neuron and astrocyte Na+-K+ ATPase pump strengths. In particular, we consider the neuroprotective role of astrocyte gap junction coupling. The model demonstrates that a syncytium of electrically coupled astrocytes can maintain a physiological membrane potential in the presence of an elevated extracellular K+ concentration and efficiently distribute the excess K+ across the syncytium. This provides an effective neuroprotective mechanism for delaying or preventing the initiation of spreading depolarizations.

Biological inspired simulation of neuron-astrocyte networks

Biological inspired simulation of neuron-astrocyte networks

Multiplier-less digital implementation of neuron–astrocyte signalling on FPGA

Experimental observations have shown that astrocytes are active partner in neural information processing which are mainly carried out by neurons. In this research, we investigate this issue and provide a computationally efficient digital circuit for neuron–astrocyte interactions. The firing dynamics of the neuron is described by Izhikevich model (spiking and bursting activities) and the calcium dynamics of a single astrocyte explained by a proposed model adapted from a functional model introduced by Postnov and colleagues. The new linear model makes it possible to design an efficient multiplier-less hardware architecture for digital implementation of neuron–astrocyte interaction on field-programmable gate array (FPGA). Using the proposed neuron–astrocyte circuit and based on the results of MATLAB simulation, hardware synthesis and FPGA implementation, it is demonstrated that the proposed digital astrocyte is able to change the neuron spiking frequency through bidirectional signaling. This circuit may represent a fundamental computational unit for the development of artificial neuron–astrocyte networks, opening new perspectives in pattern recognition tasks.

Mechanisms Involved in Dual Vasopressin/Apelin Neuron Dysfunction during Aging

Normal aging is associated with vasopressin neuron adaptation, but little is known about its effects on the release of apelin, an aquaretic peptide colocalized with vasopressin. We found that plasma vasopressin concentrations were higher and plasma apelin concentrations lower in aged rats than in younger adults. The response of AVP/apelin neurons to osmotic challenge was impaired in aged rats. The overactivity of vasopressin neurons was sustained partly by the increased expression of Transient receptor potential vanilloid2 (Trpv2), because central Trpv blocker injection reversed the age-induced increase in plasma vasopressin concentration without modifying plasma apelin concentration. The morphofunctional plasticity of the supraoptic nucleus neuron-astrocyte network normally observed during chronic dehydration in adults appeared to be impaired in aged rats as well. IL-6 overproduction by astrocytes and low-grade microglial neuroinflammation may contribute to the modification of neuronal functioning during aging. Indeed, central treatment with antibodies against IL-6 decreased plasma vasopressin levels and increased plasma apelin concentration toward the values observed in younger adults. Conversely, minocycline treatment (inhibiting microglial metabolism) did not affect plasma vasopressin concentration, but increased plasma apelin concentration toward control values for younger adults. This study is the first to demonstrate dual vasopressin/apelin adaptation mediated by inflammatory molecules and neuronal Trpv2, during aging.

Dynamical patterns of calcium signaling in a functional model of neuron–astrocyte networks

We propose a functional mathematical model for neuron-astrocyte networks. The model incorporates elements of the tripartite synapse and the spatial branching structure of coupled astrocytes. We consider glutamate-induced calcium signaling as a specific mode of excitability and transmission in astrocytic-neuronal networks. We reproduce local and global dynamical patterns observed experimentally.

Rapid Astrocyte Calcium Signals Correlate with Neuronal Activity and Onset of the Hemodynamic Response In Vivo

Elevation of intracellular Ca2+ in astrocytes can influence cerebral microcirculation and modulate synaptic transmission. Recently, in vivo imaging studies identified delayed, sensory-driven Ca2+ oscillations in cortical astrocytes; however, the long latencies of these Ca2+ signals raises questions in regards to their suitability for a role in short-latency modulation of cerebral microcirculation or rapid astrocyte-to-neuron communication. Here, using in vivo two-photon Ca2+ imaging, we demonstrate that approximately 5% of sulforhodamine 101-labeled astrocytes in the hindlimb area of the mouse primary somatosensory cortex exhibit short-latency (peak amplitude approximately 0.5 s after stimulus onset), contralateral hindlimb-selective sensory-evoked Ca2+ signals that operate on a time scale similar to neuronal activity and correlate with the onset of the hemodynamic response as measured by intrinsic signal imaging. The kinetics of astrocyte Ca2+ transients were similar in rise and decay times to postsynaptic neuronal transients, but decayed more slowly than neuropil Ca2+ transients that presumably reflect presynaptic transients. These in vivo findings suggest that astrocytes can respond to sensory activity in a selective manner and process information on a subsecond time scale, enabling them to potentially form an active partnership with neurons for rapid regulation of microvascular tone and neuron-astrocyte network properties.