Selectivity and Metaplasticity in a Unified Calcium-Dependent Model

A unified, biophysically motivated Calcium-Dependent Learning model has been shown to account for various rate-based and spike time-dependent paradigms for inducing synaptic plasticity. Here, we investigate the properties of this model for a multi-synapse neuron that receives inputs with different spike-train statistics. In addition, we present a physiological form of metaplasticity, an activity-driven regulation mechanism, that is essential for the robustness of the model. A neuron thus implemented develops stable and selective receptive fields, given various input statistic

Excitatory, Inhibitory, and Structural Plasticity Produce Correlated Connectivity in Random Networks Trained to Solve Paired-Stimulus Tasks

The pattern of connections among cortical excitatory cells with overlapping arbors is non-random. In particular, correlations among connections produce clustering – cells in cliques connect to each other with high probability, but with lower probability to cells in other spatially intertwined cliques. In this study, we model initially randomly connected sparse recurrent networks of spiking neurons with random, overlapping inputs, to investigate what functional and structural synaptic plasticity mechanisms sculpt network connections into the patterns measured in vitro. Our Hebbian implementation of structural plasticity causes a removal of connections between uncorrelated excitatory cells, followed by their random replacement. To model a biconditional discrimination task, we stimulate the network via pairs (A + B, C + D, A + D, and C + B) of four inputs (A, B, C, and D). We find networks that produce neurons most responsive to specific paired inputs – a building block of computation and essential role for cortex – contain the excessive clustering of excitatory synaptic connections observed in cortical slices. The same networks produce the best performance in a behavioral readout of the networks’ ability to complete the task. A plasticity mechanism operating on inhibitory connections, long-term potentiation of inhibition, when combined with structural plasticity, indirectly enhances clustering of excitatory cells via excitatory connections. A rate-dependent (triplet) form of spike-timing-dependent plasticity (STDP) between excitatory cells is less effective and basic STDP is detrimental. Clustering also arises in networks stimulated with single stimuli and in networks undergoing raised levels of spontaneous activity when structural plasticity is combined with functional plasticity. In conclusion, spatially intertwined clusters or cliques of connected excitatory cells can arise via a Hebbian form of structural plasticity operating in initially randomly connected networks

Neuromodulation of Spike-Timing-Dependent Plasticity: Past, Present, and Future.

Spike-timing-dependent synaptic plasticity (STDP) is a leading cellular model for behavioral learning and memory with rich computational properties. However, the relationship between the millisecond-precision spike timing required for STDP and the much slower timescales of behavioral learning is not well understood. Neuromodulation offers an attractive mechanism to connect these different timescales, and there is now strong experimental evidence that STDP is under neuromodulatory control by acetylcholine, monoamines, and other signaling molecules. Here, we review neuromodulation of STDP, the underlying mechanisms, functional implications, and possible involvement in brain disorders.BBSR

Synaptic and nonsynaptic plasticity approximating probabilistic inference

Learning and memory operations in neural circuits are believed to involve molecular cascades of synaptic and nonsynaptic changes that lead to a diverse repertoire of dynamical phenomena at higher levels of processing. Hebbian and homeostatic plasticity, neuromodulation, and intrinsic excitability all conspire to form and maintain memories. But it is still unclear how these seemingly redundant mechanisms could jointly orchestrate learning in a more unified system. To this end, a Hebbian learning rule for spiking neurons inspired by Bayesian statistics is proposed. In this model, synaptic weights and intrinsic currents are adapted on-line upon arrival of single spikes, which initiate a cascade of temporally interacting memory traces that locally estimate probabilities associated with relative neuronal activation levels. Trace dynamics enable synaptic learning to readily demonstrate a spike-timing dependence, stably return to a set-point over long time scales, and remain competitive despite this stability. Beyond unsupervised learning, linking the traces with an external plasticity-modulating signal enables spike-based reinforcement learning. At the postsynaptic neuron, the traces are represented by an activity-dependent ion channel that is shown to regulate the input received by a postsynaptic cell and generate intrinsic graded persistent firing levels. We show how spike-based Hebbian-Bayesian learning can be performed in a simulated inference task using integrate-and-fire (IAF) neurons that are Poisson-firing and background-driven, similar to the preferred regime of cortical neurons. Our results support the view that neurons can represent information in the form of probability distributions, and that probabilistic inference could be a functional by-product of coupled synaptic and nonsynaptic mechanisms operating over several timescales. The model provides a biophysical realization of Bayesian computation by reconciling several observed neural phenomena whose functional effects are only partially understood in concert.This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission.QC 20150430BrainScaleSErasmus Mundus EuroSPI

The hippocampus and cerebellum in adaptively timed learning, recognition, and movement

The concepts of declarative memory and procedural memory have been used to distinguish two basic types of learning. A neural network model suggests how such memory processes work together as recognition learning, reinforcement learning, and sensory-motor learning take place during adaptive behaviors. To coordinate these processes, the hippocampal formation and cerebellum each contain circuits that learn to adaptively time their outputs. Within the model, hippocampal timing helps to maintain attention on motivationally salient goal objects during variable task-related delays, and cerebellar timing controls the release of conditioned responses. This property is part of the model's description of how cognitive-emotional interactions focus attention on motivationally valued cues, and how this process breaks down due to hippocampal ablation. The model suggests that the hippocampal mechanisms that help to rapidly draw attention to salient cues could prematurely release motor commands were not the release of these commands adaptively timed by the cerebellum. The model hippocampal system modulates cortical recognition learning without actually encoding the representational information that the cortex encodes. These properties avoid the difficulties faced by several models that propose a direct hippocampal role in recognition learning. Learning within the model hippocampal system controls adaptive timing and spatial orientation. Model properties hereby clarify how hippocampal ablations cause amnesic symptoms and difficulties with tasks which combine task delays, novelty detection, and attention towards goal objects amid distractions. When these model recognition, reinforcement, sensory-motor, and timing processes work together, they suggest how the brain can accomplish conditioning of multiple sensory events to delayed rewards, as during serial compound conditioning.Air Force Office of Scientific Research (F49620-92-J-0225, F49620-86-C-0037, 90-0128); Advanced Research Projects Agency (ONR N00014-92-J-4015); Office of Naval Research (N00014-91-J-4100, N00014-92-J-1309, N00014-92-J-1904); National Institute of Mental Health (MH-42900

Modeling the Bat Spatial Navigation System: A Neuromorphic VLSI Approach

Autonomously navigating robots have long been a tough challenge facing engineers. The recent push to develop micro-aerial vehicles for practical military, civilian, and industrial use has added a significant power and time constraint to the challenge. In contrast, animals, from insects to humans, have been navigating successfully for millennia using a wide range of variants of the ultra-low-power computational system known as the brain. For this reason, we look to biological systems to inspire a solution suitable for autonomously navigating micro-aerial vehicles. In this dissertation, the focus is on studying the neurobiological structures involved in mammalian spatial navigation. The mammalian brain areas widely believed to contribute directly to navigation tasks are the Head Direction Cells, Grid Cells and Place Cells found in the post-subiculum, the medial entorhinal cortex, and the hippocampus, respectively. In addition to studying the neurobiological structures involved in navigation, we investigate various neural models that seek to explain the operation of these structures and adapt them to neuromorphic VLSI circuits and systems. We choose the neuromorphic approach for our systems because we are interested in understanding the interaction between the real-time, physical implementation of the algorithms and the real-world problem (robot and environment). By utilizing both analog and asynchronous digital circuits to mimic similar computations in neural systems, we envision very low power VLSI implementations suitable for providing practical solutions for spatial navigation in micro-aerial vehicles

Coding and learning of chemosensor array patterns in a neurodynamic model of the olfactory system

Arrays of broadly-selective chemical sensors, also known as electronic noses, have been developed during the past two decades as a low-cost and high-throughput alternative to analytical instruments for the measurement of odorant chemicals. Signal processing in these gas-sensor arrays has been traditionally performed by means of statistical and neural pattern recognition techniques. The objective of this dissertation is to develop new computational models to process gas sensor array signals inspired by coding and learning mechanisms of the biological olfactory system. We have used a neurodynamic model of the olfactory system, the KIII, to develop and demonstrate four odor processing computational functions: robust recovery of overlapping patterns, contrast enhancement, background suppression, and novelty detection. First, a coding mechanism based on the synchrony of neural oscillations is used to extract information from the associative memory of the KIII model. This temporal code allows the KIII to recall overlapping patterns in a robust manner. Second, a new learning rule that combines Hebbian and anti-Hebbian terms is proposed. This learning rule is shown to achieve contrast enhancement on gas-sensor array patterns. Third, a new local learning mechanism based on habituation is proposed to perform odor background suppression. Combining the Hebbian/anti-Hebbian rule and the local habituation mechanism, the KIII is able to suppress the response to continuously presented odors, facilitating the detection of the new ones. Finally, a new learning mechanism based on anti-Hebbian learning is proposed to perform novelty detection. This learning mechanism allows the KIII to detect the introduction of new odors even in the presence of strong backgrounds. The four computational models are characterized with synthetic data and validated on gas sensor array patterns obtained from an e-nose prototype developed for this purpose

Homeostatische Plastizität - algorithmische und klinische Konsequenzen

Plasticity supports the remarkable adaptability and robustness of cortical processing. It allows the brain to learn and remember patterns in the sensory world, to refine motor control, to predict and obtain reward, or to recover function after injury. Behind this great flexibility hide a range of plasticity mechanisms, affecting different aspects of neuronal communication. However, little is known about the precise computational roles of some of these mechanisms. Here, we show that the interaction between spike-timing dependent plasticity (STDP), intrinsic plasticity and synaptic scaling enables neurons to learn efficient representations of their inputs. In the context of reward-dependent learning, the same mechanisms allow a neural network to solve a working memory task. Moreover, although we make no any apriori assumptions on the encoding used for representing inputs, the network activity resembles that of brain regions known to be associated with working memory, suggesting that reward-dependent learning may be a central force in working memory development. Lastly, we investigated some of the clinical implications of synaptic scaling and showed that, paradoxically, there are situations in which the very mechanisms that normally are required to preserve the balance of the system, may act as a destabilizing factor and lead to seizures. Our model offers a novel explanation for the increased incidence of seizures following chronic inflammation.Das menschliche Gehirn ist in der Lage sich an dramatische Veränderungen der Umgebung anzupassen. Hinter der Anpassungsfähigkeit des Gehirns stecken verschiedenste ernmechanismen. Einige dieser Mechanismen sind bereits relativ gut erforscht, wahrend bei anderen noch kaum bekannt ist, welche Rolle sie innerhalb der Informationsverarbeitungsprozesse im Gehirn spielen. Hier, soll gezeigt werden, dass das Zusammenspiel von Spike-Timing Dependent Plasticity' (STDP) mit zwei weiteren Prozessen, Synaptic Scaling' und Intrinsic Plasticity' (IP), es Nervenzellen ermöglicht Information effizient zu kodieren. Die gleichen Mechanismen führen dazu, dass ein Netzwerk aus Neuronen in der Lage ist, ein Arbeitsgedächtnis' für vergangene Stimuli zu entwickeln. Durch die Kombination von belohnungsabhängigem STDP und homöostatischen Mechanismen lernt das Netzwerk, die Stimulus-Repräsentationen für mehrere Zeitschritte verfügbar zu halten. Obwohl in unserem Modell-Design keinerlei. Informationen über die bevorzugte Art der Kodierung enthalten sind, finden wir nach Ende des Trainings neuronale Repräsentationen, die denjenigen aus vielen Arbeitsgedächtnis-Experimenten gleichen. Unser Modell zeigt, dass solche Repräsentationen durch Lernen enstehen können und dass Reward-abhängige Prozesse eine zentrale Kraft bei der Entwicklung des Arbeitsgedächtnisses spielen können. Abschliessend werden klinische Konsequenzen einiger Lern-Prozesse untersucht. Wir konnten zeigen, dass der selbe Mechanismus, der normalerweise die Aktivität im Gehirn in Balance hält, in speziellen Situationen auch zu Destabilisierung führen und epileptische Anfälle auslösen kann. Das hier vorgestellte Modell liefert eine neuartige Erklärung zur Entstehung von epileptischen Anfällen bei chronischen Entzündungen

Spike-based local synaptic plasticity: a survey of computational models and neuromorphic circuits

Understanding how biological neural networks carry out learning using spike-based local plasticity mechanisms can lead to the development of real-time, energy-efficient, and adaptive neuromorphic processing systems. A large number of spike-based learning models have recently been proposed following different approaches. However, it is difficult to assess if these models can be easily implemented in neuromorphic hardware, and to compare their features and ease of implementation. To this end, in this survey, we provide an overview of representative brain-inspired synaptic plasticity models and mixed-signal complementary metal–oxide–semiconductor neuromorphic circuits within a unified framework. We review historical, experimental, and theoretical approaches to modeling synaptic plasticity, and we identify computational primitives that can support low-latency and low-power hardware implementations of spike-based learning rules. We provide a common definition of a locality principle based on pre- and postsynaptic neural signals, which we propose as an important requirement for physical implementations of synaptic plasticity circuits. Based on this principle, we compare the properties of these models within the same framework, and describe a set of mixed-signal electronic circuits that can be used to implement their computing principles, and to build efficient on-chip and online learning in neuromorphic processing systems