859 research outputs found

    Unstable Dynamics, Nonequilibrium Phases and Criticality in Networked Excitable Media

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    Here we numerically study a model of excitable media, namely, a network with occasionally quiet nodes and connection weights that vary with activity on a short-time scale. Even in the absence of stimuli, this exhibits unstable dynamics, nonequilibrium phases -including one in which the global activity wanders irregularly among attractors- and 1/f noise while the system falls into the most irregular behavior. A net result is resilience which results in an efficient search in the model attractors space that can explain the origin of certain phenomenology in neural, genetic and ill-condensed matter systems. By extensive computer simulation we also address a relation previously conjectured between observed power-law distributions and the occurrence of a "critical state" during functionality of (e.g.) cortical networks, and describe the precise nature of such criticality in the model.Comment: 18 pages, 9 figure

    Short term synaptic depression improves information transfer in perceptual multistability

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    Competitive neural networks are often used to model the dynamics of perceptual bistability. Switching between percepts can occur through fluctuations and/or a slow adaptive process. Here, we analyze switching statistics in competitive networks with short term synaptic depression and noise. We start by analyzing a ring model that yields spatially structured solutions and complement this with a study of a space-free network whose populations are coupled with mutual inhibition. Dominance times arising from depression driven switching can be approximated using a separation of timescales in the ring and space-free model. For purely noise-driven switching, we use energy arguments to justify how dominance times are exponentially related to input strength. We also show that a combination of depression and noise generates realistic distributions of dominance times. Unimodal functions of dominance times are more easily differentiated from one another using Bayesian sampling, suggesting synaptic depression induced switching transfers more information about stimuli than noise-driven switching. Finally, we analyze a competitive network model of perceptual tristability, showing depression generates a memory of previous percepts based on the ordering of percepts.Comment: 26 pages, 15 figure

    Anergy in self-directed B lymphocytes from a statistical mechanics perspective

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    The ability of the adaptive immune system to discriminate between self and non-self mainly stems from the ontogenic clonal-deletion of lymphocytes expressing strong binding affinity with self-peptides. However, some self-directed lymphocytes may evade selection and still be harmless due to a mechanism called clonal anergy. As for B lymphocytes, two major explanations for anergy developed over three decades: according to "Varela theory", it stems from a proper orchestration of the whole B-repertoire, in such a way that self-reactive clones, due to intensive interactions and feed-back from other clones, display more inertia to mount a response. On the other hand, according to the `two-signal model", which has prevailed nowadays, self-reacting cells are not stimulated by helper lymphocytes and the absence of such signaling yields anergy. The first result we present, achieved through disordered statistical mechanics, shows that helper cells do not prompt the activation and proliferation of a certain sub-group of B cells, which turn out to be just those broadly interacting, hence it merges the two approaches as a whole (in particular, Varela theory is then contained into the two-signal model). As a second result, we outline a minimal topological architecture for the B-world, where highly connected clones are self-directed as a natural consequence of an ontogenetic learning; this provides a mathematical framework to Varela perspective. As a consequence of these two achievements, clonal deletion and clonal anergy can be seen as two inter-playing aspects of the same phenomenon too

    An associative memory of Hodgkin-Huxley neuron networks with Willshaw-type synaptic couplings

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    An associative memory has been discussed of neural networks consisting of spiking N (=100) Hodgkin-Huxley (HH) neurons with time-delayed couplings, which memorize P patterns in their synaptic weights. In addition to excitatory synapses whose strengths are modified after the Willshaw-type learning rule with the 0/1 code for quiescent/active states, the network includes uniform inhibitory synapses which are introduced to reduce cross-talk noises. Our simulations of the HH neuron network for the noise-free state have shown to yield a fairly good performance with the storage capacity of αc=Pmax/N0.42.4\alpha_c = P_{\rm max}/N \sim 0.4 - 2.4 for the low neuron activity of f0.040.10f \sim 0.04-0.10. This storage capacity of our temporal-code network is comparable to that of the rate-code model with the Willshaw-type synapses. Our HH neuron network is realized not to be vulnerable to the distribution of time delays in couplings. The variability of interspace interval (ISI) of output spike trains in the process of retrieving stored patterns is also discussed.Comment: 15 pages, 3 figures, changed Titl

    Epigenetic Landscapes Explain Partially Reprogrammed Cells and Identify Key Reprogramming Genes

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    A common metaphor for describing development is a rugged “epigenetic landscape” where cell fates are represented as attracting valleys resulting from a complex regulatory network. Here, we introduce a framework for explicitly constructing epigenetic landscapes that combines genomic data with techniques from spin-glass physics. Each cell fate is a dynamic attractor, yet cells can change fate in response to external signals. Our model suggests that partially reprogrammed cells are a natural consequence of high-dimensional landscapes, and predicts that partially reprogrammed cells should be hybrids that co-express genes from multiple cell fates. We verify this prediction by reanalyzing existing datasets. Our model reproduces known reprogramming protocols and identifies candidate transcription factors for reprogramming to novel cell fates, suggesting epigenetic landscapes are a powerful paradigm for understanding cellular identity
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