In recent years research suggests that astrocyte networks, in addition to nutrient and waste processing functions, regulate both structural and synaptic plasticity. To understand the biological mechanisms that underpin such plasticity requires the development of cell level models that capture the mutual interaction between astrocytes and neurons. This paper presents a detailed model of bidirectional signaling between astrocytes and neurons (the astrocyte-neuron model or AN model) which yields new insights into the computational role of astrocyte-neuronal coupling. From a set of modeling studies we demonstrate two significant findings. Firstly, that spatial signaling via astrocytes can relay a “learning signal” to remote synaptic sites. Results show that slow inward currents cause synchronized postsynaptic activity in remote neurons and subsequently allow Spike-Timing-Dependent Plasticity based learning to occur at the associated synapses. Secondly, that bidirectional communication between neurons and astrocytes underpins dynamic coordination between neuron clusters. Although our composite AN model is presently applied to simplified neural structures and limited to coordination between localized neurons, the principle (which embodies structural, functional and dynamic complexity), and the modeling strategy may be extended to coordination among remote neuron clusters.

Spiking neural networks (SNNs) attempt to emulate information processing in the mammalian brain based on massively parallel arrays of neurons that communicate via spike events. SNNs offer the possibility to implement embedded neuromorphic circuits, with high parallelism and low power consumption compared to the traditional von Neumann computer paradigms. Nevertheless, the lack of modularity and poor connectivity shown by traditional neuron interconnect implementations based on shared bus topologies is prohibiting scalable hardware implementations of SNNs. This paper presents a novel hierarchical network-on-chip (H-NoC) architecture for SNN hardware, which aims to address the scalability issue by creating a modular array of clusters of neurons using a hierarchical structure of low and high-level routers. The proposed H-NoC architecture incorporates a spike traffic compression technique to exploit SNN traffic patterns and locality between neurons, thus reducing traffic overhead and improving throughput on the network. In addition, adaptive routing capabilities between clusters balance local and global traffic loads to sustain throughput under bursting activity. Analytical results show the scalability of the proposed H-NoC approach under different scenarios, while simulation and synthesis analysis using 65-nm CMOS technology demonstrate high-throughput, low-cost area, and power consumption per cluster, respectively.

A biophysical model that captures molecular homeostatic control of ions at the perisynaptic cradle (PsC) is of fundamental importance for understanding the interplay between astroglial and neuronal compartments. In this paper, we develop a multi-compartmental mathematical model which proposes a novel mechanism whereby the flow of cations in thin processes is restricted due to negatively charged membrane lipids which result in the formation of deep potential wells near the dipole heads. These wells restrict the flow of cations to “hopping” between adjacent wells as they transverse the process, and this surface retention of cations will be shown to give rise to the formation of potassium (K⁺) and sodium (Na⁺) microdomains at the PsC. We further propose that a K⁺ microdomain formed at the PsC, provides the driving force for the return of K⁺ to the extracellular space for uptake by the neurone, thereby preventing K⁺ undershoot. A slow decay of Na⁺ was also observed in our simulation after a period of glutamate stimulation which is in strong agreement with experimental observations. The pathological implications of microdomain formation during neuronal excitation are also discussed. During periods of neuronal activity, ionic homeostasis in the surrounding extracellular space (ECS) is disturbed. To provide a healthy environment for continued neuronal function, excess ions such as potassium must be buffered away from the ECS; a vital supportive role provided by astrocyte cells. It has long been thought that astrocytes not only removed ions from the ECS but also transport them to other areas of the brain where their concentrations are lower. However, while our computational model simulations agree that astrocytes do remove these ions from the ECS they also show that these ions are mainly stored locally at the PsC to be returned to the ECS, thus restoring ionic homeostasis. Furthermore, we detail in this paper that this happens because of a previously overlooked biophysical phenomenon that is only dominant in thin astrocyte processes. The flow of these cations within thin processes is primarily by surface conduction where they experience the attraction of fixed negative charge at the membrane inner surface. This negative charge constrains cation movement along the surface and so their flow rate is restricted. Consequently, ions such as potassium that are released during neuronal excitation enter the PsC and are stored locally due to the low conductance pathway between the PsC and the astrocyte soma. Our simulations also show that this local build-up of K⁺ is returned to the ECS after the neuronal activity dies off which could potentially explain why K⁺ undershoot has not been observed; this result agrees with experimental observations. Moreover, the same mechanism can also explain the transient behaviour of Na⁺ ions whereby in thin processes a slow decay time constant is experimentally observed. These findings have important implications for the role of astrocytes in regulating neuronal excitability under physiological and pathological conditions, and therefore highlight the significance of the work presented in this paper.

Recent research has shown that a glial cell of astrocyte underpins a self-repair mechanism in the human brain, where spiking neurons provide direct and indirect feedbacks to presynaptic terminals. These feedbacks modulate the synaptic transmission probability of release (PR). When synaptic faults occur, the neuron becomes silent or near silent due to the low PR of synapses; whereby the PRs of remaining healthy synapses are then increased by the indirect feedback from the astrocyte cell. In this paper, a novel hardware architecture of Self-rePAiring spiking Neural NEtwoRk (SPANNER) is proposed, which mimics this self-repairing capability in the human brain. This paper demonstrates that the hardware can self-detect and self-repair synaptic faults without the conventional components for the fault detection and fault repairing. Experimental results show that SPANNER can maintain the system performance with fault densities of up to 40%, and more importantly SPANNER has only a 20% performance degradation when the self-repairing architecture is significantly damaged at a fault density of 80%.