Network Plasticity as Bayesian Inference

General results from statistical learning theory suggest to understand not only brain computations, but also brain plasticity as probabilistic inference. But a model for that has been missing. We propose that inherently stochastic features of synaptic plasticity and spine motility enable cortical networks of neurons to carry out probabilistic inference by sampling from a posterior distribution of network configurations. This model provides a viable alternative to existing models that propose convergence of parameters to maximum likelihood values. It explains how priors on weight distributions and connection probabilities can be merged optimally with learned experience, how cortical networks can generalize learned information so well to novel experiences, and how they can compensate continuously for unforeseen disturbances of the network. The resulting new theory of network plasticity explains from a functional perspective a number of experimental data on stochastic aspects of synaptic plasticity that previously appeared to be quite puzzling.Comment: 33 pages, 5 figures, the supplement is available on the author's web page http://www.igi.tugraz.at/kappe

A dynamic system approach to spiking second order memristor networks

Second order memristors are two terminal devices that present a conductance depending on two orders of variables, namely the geometric parameters and the internal temperature. They have shown to be able to mimic some specific features of neuron synapses, specifically Spike-Timing-Dependent-Plasticity (STDP), and consequently to be good candidates for neuromor- phic computing. In particular, memristor crossbar structures appear to be suitable for implementing locally competitive algorithms and for tackling classification problems by exploiting temporal learning techniques. On the other hand, neuromorphic studies and experiments have revealed the existence of differ- ent kinds of plasticity and have shown the effect of calcium concentration on synaptic changes. Computational studies have investigated the behavior of spiking networks in the context of supervised, unsupervised, and reinforcement learning. In this paper, we first derive a simplified, almost analytical, model of a second-order memristor, only involving two variables, the mem- conductance, and the temperature, directly attributable to the synaptic efficacy and to the calcium concentration. Then we study in detail the response of a single memristive synapse to the most relevant plasticity models, including cycles of spike pairs, triplets, and quadruplets at different frequencies. Finally, we accurately characterize memristor spiking networks as discrete nonlinear dynamic systems, with mem-conductances as state variables and pre and postsynaptic spikes as inputs and outputs, respectively. The result shows that the model developed in this manuscript can explain and accurately reproduce a significant portion of observed synaptic behaviors, including those not captured by classical spike pair-based STDP models. Furthermore, under such an approach, the global dynamic behavior of memristor networks and the related learning mechanisms can be deeply analyzed by employing advanced nonlinear dynamic techniques

Learning to Discriminate Through Long-Term Changes of Dynamical Synaptic Transmission

Short-term synaptic plasticity is modulated by long-term synaptic changes. There is, however, no general agreement on the computational role of this interaction. Here, we derive a learning rule for the release probability and the maximal synaptic conductance in a circuit model with combined recurrent and feedforward connections that allows learning to discriminate among natural inputs. Short-term synaptic plasticity thereby provides a nonlinear expansion of the input space of a linear classifier, whereas the random recurrent network serves to decorrelate the expanded input space. Computer simulations reveal that the twofold increase in the number of input dimensions through short-term synaptic plasticity improves the performance of a standard perceptron up to 100%. The distributions of release probabilities and maximal synaptic conductances at the capacity limit strongly depend on the balance between excitation and inhibition. The model also suggests a new computational interpretation of spikes evoked by stimuli outside the classical receptive field. These neuronal activitiesmay reflect decorrelation of the expanded stimulus space by intracortical synaptic connections

Homeostatic plasticity and external input shape neural network dynamics

In vitro and in vivo spiking activity clearly differ. Whereas networks in vitro develop strong bursts separated by periods of very little spiking activity, in vivo cortical networks show continuous activity. This is puzzling considering that both networks presumably share similar single-neuron dynamics and plasticity rules. We propose that the defining difference between in vitro and in vivo dynamics is the strength of external input. In vitro, networks are virtually isolated, whereas in vivo every brain area receives continuous input. We analyze a model of spiking neurons in which the input strength, mediated by spike rate homeostasis, determines the characteristics of the dynamical state. In more detail, our analytical and numerical results on various network topologies show consistently that under increasing input, homeostatic plasticity generates distinct dynamic states, from bursting, to close-to-critical, reverberating and irregular states. This implies that the dynamic state of a neural network is not fixed but can readily adapt to the input strengths. Indeed, our results match experimental spike recordings in vitro and in vivo: the in vitro bursting behavior is consistent with a state generated by very low network input (< 0.1%), whereas in vivo activity suggests that on the order of 1% recorded spikes are input-driven, resulting in reverberating dynamics. Importantly, this predicts that one can abolish the ubiquitous bursts of in vitro preparations, and instead impose dynamics comparable to in vivo activity by exposing the system to weak long-term stimulation, thereby opening new paths to establish an in vivo-like assay in vitro for basic as well as neurological studies.Comment: 14 pages, 8 figures, accepted at Phys. Rev.

Astrocytes: Orchestrating synaptic plasticity?

Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neural activity. Because synaptic plasticity is the major candidate mechanism for learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. In particular, a prominent aspect that remains debated is how the plasticity mechanisms, that encompass a broad spectrum of temporal and spatial scales, come to play together in a concerted fashion. Here we review and discuss evidence that pinpoints to a possible non-neuronal, glial candidate for such orchestration: the regulation of synaptic plasticity by astrocytes

Distributed ARTMAP

Distributed coding at the hidden layer of a multi-layer perceptron (MLP) endows the network with memory compression and noise tolerance capabilities. However, an MLP typically requires slow off-line learning to avoid catastrophic forgetting in an open input environment. An adaptive resonance theory (ART) model is designed to guarantee stable memories even with fast on-line learning. However, ART stability typically requires winner-take-all coding, which may cause category proliferation in a noisy input environment. Distributed ARTMAP (dARTMAP) seeks to combine the computational advantages of MLP and ART systems in a real-time neural network for supervised learning. This system incorporates elements of the unsupervised dART model as well as new features, including a content-addressable memory (CAM) rule. Simulations show that dARTMAP retains fuzzy ARTMAP accuracy while significantly improving memory compression. The model's computational learning rules correspond to paradoxical cortical data.Office of Naval Research (N00014-95-1-0409, N00014-95-1-0657

Astrocytes: orchestrating synaptic plasticity?

Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neural activity. Because synaptic plasticity is the major candidate mechanism for learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. In particular, a prominent aspect that remains debated is how the plasticity mechanisms, that encompass a broad spectrum of temporal and spatial scales, come to play together in a concerted fashion. Here we review and discuss evidence that pinpoints to a possible non-neuronal, glial candidate for such orchestration: the regulation of synaptic plasticity by astrocytes.Comment: 63 pages, 4 figure