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

Cortical free association dynamics: distinct phases of a latching network

A Potts associative memory network has been proposed as a simplified model of macroscopic cortical dynamics, in which each Potts unit stands for a patch of cortex, which can be activated in one of S local attractor states. The internal neuronal dynamics of the patch is not described by the model, rather it is subsumed into an effective description in terms of graded Potts units, with adaptation effects both specific to each attractor state and generic to the patch. If each unit, or patch, receives effective (tensor) connections from C other units, the network has been shown to be able to store a large number p of global patterns, or network attractors, each with a fraction a of the units active, where the critical load p_c scales roughly like p_c ~ (C S^2)/(a ln(1/a)) (if the patterns are randomly correlated). Interestingly, after retrieving an externally cued attractor, the network can continue jumping, or latching, from attractor to attractor, driven by adaptation effects. The occurrence and duration of latching dynamics is found through simulations to depend critically on the strength of local attractor states, expressed in the Potts model by a parameter w. Here we describe with simulations and then analytically the boundaries between distinct phases of no latching, of transient and sustained latching, deriving a phase diagram in the plane w-T, where T parametrizes thermal noise effects. Implications for real cortical dynamics are briefly reviewed in the conclusions

Attractors, memory and perception

In this Thesis, the first three introductory chapters are devoted to the review of literature on contextual perception, its neural basis and network modeling of memory. In chapter 4, the first two sections give the definition of our model; and the next two sections, 4.3 and 4.4, report the original work of mine on retrieval properties of different network structures and network dynamics underlying the response to ambiguous patterns, respectively. The reported work in chapter 5 has been done in collaboration with Prof Bharathi Jagadeesh in University of Washington, and is already published in the journal \u201dCerebral Cortex\u201d. In this collaboration, Yan Liu, from the group in Seattle, carried out the recording experiments and I did the data analysis and network simulations. Chapter 6, which represents a network model for \u201dpriming\u201d and \u201dadaptation aftereffect\u201d is done by me. The works reported in 4.3, 4.5, and the whole chapter 6 are in preparation for publication

Analog Memories in a Balanced Rate-Based Network of E-I Neurons

Abstract The persistent and graded activity often observed in cortical circuits is sometimes seen as a signature of autoassociative retrieval of memories stored earlier in synaptic efficacies. However, despite decades of theoretical work on the subject, the mechanisms that support the storage and retrieval of memories remain unclear. Previous proposals concerning the dynamics of memory networks have fallen short of incorporating some key physiological constraints in a unified way. Specifically, some models violate Dale's law (i.e. allow neurons to be both excitatory and inhibitory), while some others restrict the representation of memories to a binary format, or induce recall states in which some neurons fire at rates close to saturation. We propose a novel control-theoretic framework to build functioning attractor networks that satisfy a set of relevant physiological constraints. We directly optimize networks of excitatory and inhibitory neurons to force sets of arbitrary analog patterns to become stable fixed points of the dynamics. The resulting networks operate in the balanced regime, are robust to corruptions of the memory cue as well as to ongoing noise, and incidentally explain the reduction of trial-to-trial variability following stimulus onset that is ubiquitously observed in sensory and motor cortices. Our results constitute a step forward in our understanding of the neural substrate of memory

The mechanisms for pattern completion and pattern separation in the hippocampus

The mechanisms for pattern completion and pattern separation are described in the context of a theory of hippocampal function in which the hippocampal CA3 system operates as a single attractor or autoassociation network to enable rapid, one-trial, associations between any spatial location (place in rodents, or spatial view in primates) and an object or reward, and to provide for completion of the whole memory during recall from any part. The factors important in the pattern completion in CA3 together with a large number of independent memories stored in CA3 include a sparse distributed representation which is enhanced by the graded firing rates of CA3 neurons, representations that are independent due to the randomizing effect of the mossy fibers, heterosynaptic long-term depression as well as long-term potentiation in the recurrent collateral synapses, and diluted connectivity to minimize the number of multiple synapses between any pair of CA3 neurons which otherwise distort the basins of attraction. Recall of information from CA3 is implemented by the entorhinal cortex perforant path synapses to CA3 cells, which in acting as a pattern associator allow some pattern generalization. Pattern separation is performed in the dentate granule cells using competitive learning to convert grid-like entorhinal cortex firing to place-like fields. Pattern separation in CA3, which is important for completion of any one of the stored patterns from a fragment, is provided for by the randomizing effect of the mossy fiber synapses to which neurogenesis may contribute, by the large number of dentate granule cells each with a sparse representation, and by the sparse independent representations in CA3. Recall to the neocortex is achieved by a reverse hierarchical series of pattern association networks implemented by the hippocampo-cortical backprojections, each one of which performs some pattern generalization, to retrieve a complete pattern of cortical firing in higher-order cortical areas