Connection Strategies in Associative Memory Models

“The original publication is available at www.springerlink.com”. Copyright Springer.The problem we address in this paper is that of finding effective and parsimonious patterns of connectivity in sparse associative memories. This problem must be addressed in real neuronal systems, so results in artificial systems could throw light on real systems. We show that there are efficient patterns of connectivity and that these patterns are effective in models with either spiking or non-spiking neurons. This suggests that there may be some underlying general principles governing good connectivity in such networks.Peer reviewe

Clustering Predicts Memory Performance in Networks of Spiking and Non-Spiking Neurons

The problem we address in this paper is that of finding effective and parsimonious patterns of connectivity in sparse associative memories. This problem must be addressed in real neuronal systems, so that results in artificial systems could throw light on real systems. We show that there are efficient patterns of connectivity and that these patterns are effective in models with either spiking or non-spiking neurons. This suggests that there may be some underlying general principles governing good connectivity in such networks. We also show that the clustering of the network, measured by Clustering Coefficient, has a strong negative linear correlation to the performance of associative memory. This result is important since a purely static measure of network connectivity appears to determine an important dynamic property of the network

Memory and information processing in neuromorphic systems

A striking difference between brain-inspired neuromorphic processors and current von Neumann processors architectures is the way in which memory and processing is organized. As Information and Communication Technologies continue to address the need for increased computational power through the increase of cores within a digital processor, neuromorphic engineers and scientists can complement this need by building processor architectures where memory is distributed with the processing. In this paper we present a survey of brain-inspired processor architectures that support models of cortical networks and deep neural networks. These architectures range from serial clocked implementations of multi-neuron systems to massively parallel asynchronous ones and from purely digital systems to mixed analog/digital systems which implement more biological-like models of neurons and synapses together with a suite of adaptation and learning mechanisms analogous to the ones found in biological nervous systems. We describe the advantages of the different approaches being pursued and present the challenges that need to be addressed for building artificial neural processing systems that can display the richness of behaviors seen in biological systems.Comment: Submitted to Proceedings of IEEE, review of recently proposed neuromorphic computing platforms and system

The Performance of Associative Memory Models with Biologically Inspired Connectivity

This thesis is concerned with one important question in artificial neural networks, that is, how biologically inspired connectivity of a network affects its associative memory performance. In recent years, research on the mammalian cerebral cortex, which has the main responsibility for the associative memory function in the brains, suggests that the connectivity of this cortical network is far from fully connected, which is commonly assumed in traditional associative memory models. It is found to be a sparse network with interesting connectivity characteristics such as the “small world network” characteristics, represented by short Mean Path Length, high Clustering Coefficient, and high Global and Local Efficiency. Most of the networks in this thesis are therefore sparsely connected. There is, however, no conclusive evidence of how these different connectivity characteristics affect the associative memory performance of a network. This thesis addresses this question using networks with different types of connectivity, which are inspired from biological evidences. The findings of this programme are unexpected and important. Results show that the performance of a non-spiking associative memory model is found to be predicted by its linear correlation with the Clustering Coefficient of the network, regardless of the detailed connectivity patterns. This is particularly important because the Clustering Coefficient is a static measure of one aspect of connectivity, whilst the associative memory performance reflects the result of a complex dynamic process. On the other hand, this research reveals that improvements in the performance of a network do not necessarily directly rely on an increase in the network’s wiring cost. Therefore it is possible to construct networks with high associative memory performance but relatively low wiring cost. Particularly, Gaussian distributed connectivity in a network is found to achieve the best performance with the lowest wiring cost, in all examined connectivity models. Our results from this programme also suggest that a modular network with an appropriate configuration of Gaussian distributed connectivity, both internal to each module and across modules, can perform nearly as well as the Gaussian distributed non-modular network. Finally, a comparison between non-spiking and spiking associative memory models suggests that in terms of associative memory performance, the implication of connectivity seems to transcend the details of the actual neural models, that is, whether they are spiking or non-spiking neurons

Improving Associative Memory in a Network of Spiking Neurons

In this thesis we use computational neural network models to examine the dynamics and functionality of the CA3 region of the mammalian hippocampus. The emphasis of the project is to investigate how the dynamic control structures provided by inhibitory circuitry and cellular modification may effect the CA3 region during the recall of previously stored information. The CA3 region is commonly thought to work as a recurrent auto-associative neural network due to the neurophysiological characteristics found, such as, recurrent collaterals, strong and sparse synapses from external inputs and plasticity between coactive cells. Associative memory models have been developed using various configurations of mathematical artificial neural networks which were first developed over 40 years ago. Within these models we can store information via changes in the strength of connections between simplified model neurons (two-state). These memories can be recalled when a cue (noisy or partial) is instantiated upon the net. The type of information they can store is quite limited due to restrictions caused by the simplicity of the hard-limiting nodes which are commonly associated with a binary activation threshold. We build a much more biologically plausible model with complex spiking cell models and with realistic synaptic properties between cells. This model is based upon some of the many details we now know of the neuronal circuitry of the CA3 region. We implemented the model in computer software using Neuron and Matlab and tested it by running simulations of storage and recall in the network. By building this model we gain new insights into how different types of neurons, and the complex circuits they form, actually work. The mammalian brain consists of complex resistive-capacative electrical circuitry which is formed by the interconnection of large numbers of neurons. A principal cell type is the pyramidal cell within the cortex, which is the main information processor in our neural networks. Pyramidal cells are surrounded by diverse populations of interneurons which have proportionally smaller numbers compared to the pyramidal cells and these form connections with pyramidal cells and other inhibitory cells. By building detailed computational models of recurrent neural circuitry we explore how these microcircuits of interneurons control the flow of information through pyramidal cells and regulate the efficacy of the network. We also explore the effect of cellular modification due to neuronal activity and the effect of incorporating spatially dependent connectivity on the network during recall of previously stored information. In particular we implement a spiking neural network proposed by Sommer and Wennekers (2001). We consider methods for improving associative memory recall using methods inspired by the work by Graham and Willshaw (1995) where they apply mathematical transforms to an artificial neural network to improve the recall quality within the network. The networks tested contain either 100 or 1000 pyramidal cells with 10% connectivity applied and a partial cue instantiated, and with a global pseudo-inhibition.We investigate three methods. Firstly, applying localised disynaptic inhibition which will proportionalise the excitatory post synaptic potentials and provide a fast acting reversal potential which should help to reduce the variability in signal propagation between cells and provide further inhibition to help synchronise the network activity. Secondly, implementing a persistent sodium channel to the cell body which will act to non-linearise the activation threshold where after a given membrane potential the amplitude of the excitatory postsynaptic potential (EPSP) is boosted to push cells which receive slightly more excitation (most likely high units) over the firing threshold. Finally, implementing spatial characteristics of the dendritic tree will allow a greater probability of a modified synapse existing after 10% random connectivity has been applied throughout the network. We apply spatial characteristics by scaling the conductance weights of excitatory synapses which simulate the loss in potential in synapses found in the outer dendritic regions due to increased resistance. To further increase the biological plausibility of the network we remove the pseudo-inhibition and apply realistic basket cell models with differing configurations for a global inhibitory circuit. The networks are configured with; 1 single basket cell providing feedback inhibition, 10% basket cells providing feedback inhibition where 10 pyramidal cells connect to each basket cell and finally, 100% basket cells providing feedback inhibition. These networks are compared and contrasted for efficacy on recall quality and the effect on the network behaviour. We have found promising results from applying biologically plausible recall strategies and network configurations which suggests the role of inhibition and cellular dynamics are pivotal in learning and memory

Simulation of networks of spiking neurons: A review of tools and strategies

We review different aspects of the simulation of spiking neural networks. We start by reviewing the different types of simulation strategies and algorithms that are currently implemented. We next review the precision of those simulation strategies, in particular in cases where plasticity depends on the exact timing of the spikes. We overview different simulators and simulation environments presently available (restricted to those freely available, open source and documented). For each simulation tool, its advantages and pitfalls are reviewed, with an aim to allow the reader to identify which simulator is appropriate for a given task. Finally, we provide a series of benchmark simulations of different types of networks of spiking neurons, including Hodgkin-Huxley type, integrate-and-fire models, interacting with current-based or conductance-based synapses, using clock-driven or event-driven integration strategies. The same set of models are implemented on the different simulators, and the codes are made available. The ultimate goal of this review is to provide a resource to facilitate identifying the appropriate integration strategy and simulation tool to use for a given modeling problem related to spiking neural networks.Comment: 49 pages, 24 figures, 1 table; review article, Journal of Computational Neuroscience, in press (2007

Hardware design of LIF with Latency neuron model with memristive STDP synapses

In this paper, the hardware implementation of a neuromorphic system is presented. This system is composed of a Leaky Integrate-and-Fire with Latency (LIFL) neuron and a Spike-Timing Dependent Plasticity (STDP) synapse. LIFL neuron model allows to encode more information than the common Integrate-and-Fire models, typically considered for neuromorphic implementations. In our system LIFL neuron is implemented using CMOS circuits while memristor is used for the implementation of the STDP synapse. A description of the entire circuit is provided. Finally, the capabilities of the proposed architecture have been evaluated by simulating a motif composed of three neurons and two synapses. The simulation results confirm the validity of the proposed system and its suitability for the design of more complex spiking neural network