Cohesive motion in one-dimensional flocking

A one-dimensional rule-based model for flocking, that combines velocity alignment and long-range centering interactions, is presented and studied. The induced cohesion in the collective motion of the self-propelled agents leads to a unique group behaviour that contrasts with previous studies. Our results show that the largest cluster of particles, in the condensed states, develops a mean velocity slower than the preferred one in the absence of noise. For strong noise, the system also develops a non-vanishing mean velocity, alternating its direction of motion stochastically. This allows us to address the directional switching phenomenon. The effects of different sources of stochasticity on the system are also discussed.Comment: 24 pages, 11 figure

Jamming transition in a homogeneous one-dimensional system: the Bus Route Model

We present a driven diffusive model which we call the Bus Route Model. The model is defined on a one-dimensional lattice, with each lattice site having two binary variables, one of which is conserved (``buses'') and one of which is non-conserved (``passengers''). The buses are driven in a preferred direction and are slowed down by the presence of passengers who arrive with rate lambda. We study the model by simulation, heuristic argument and a mean-field theory. All these approaches provide strong evidence of a transition between an inhomogeneous ``jammed'' phase (where the buses bunch together) and a homogeneous phase as the bus density is increased. However, we argue that a strict phase transition is present only in the limit lambda -> 0. For small lambda, we argue that the transition is replaced by an abrupt crossover which is exponentially sharp in 1/lambda. We also study the coarsening of gaps between buses in the jammed regime. An alternative interpretation of the model is given in which the spaces between ``buses'' and the buses themselves are interchanged. This describes a system of particles whose mobility decreases the longer they have been stationary and could provide a model for, say, the flow of a gelling or sticky material along a pipe.Comment: 17 pages Revtex, 20 figures, submitted to Phys. Rev.

Spontaneous pulsing states in an active particle system

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Schizophrenia: do all roads lead to dopamine or is this where they start? Evidence from two epidemiologically informed developmental rodent models

The idea that there is some sort of abnormality in dopamine (DA) signalling is one of the more enduring hypotheses in schizophrenia research. Opinion leaders have published recent perspectives on the aetiology of this disorder with provocative titles such as ‘Risk factors for schizophrenia—all roads lead to dopamine' or ‘The dopamine hypothesis of schizophrenia—the final common pathway'. Perhaps, the other most enduring idea about schizophrenia is that it is a neurodevelopmental disorder. Those of us that model schizophrenia developmental risk-factor epidemiology in animals in an attempt to understand how this may translate to abnormal brain function have consistently shown that as adults these animals display behavioural, cognitive and pharmacological abnormalities consistent with aberrant DA signalling. The burning question remains how can in utero exposure to specific (environmental) insults induce persistent abnormalities in DA signalling in the adult? In this review, we summarize convergent evidence from two well-described developmental animal models, namely maternal immune activation and developmental vitamin D deficiency that begin to address this question. The adult offspring resulting from these two models consistently reveal locomotor abnormalities in response to DA-releasing or -blocking drugs. Additionally, as adults these animals have DA-related attentional and/or sensorimotor gating deficits. These findings are consistent with many other developmental animal models. However, the authors of this perspective have recently refocused their attention on very early aspects of DA ontogeny and describe reductions in genes that induce or specify dopaminergic phenotype in the embryonic brain and early changes in DA turnover suggesting that the origins of these behavioural abnormalities in adults may be traced to early alterations in DA ontogeny. Whether the convergent findings from these two models can be extended to other developmental animal models for this disease is at present unknown as such early brain alterations are rarely examined. Although it is premature to conclude that such mechanisms could be operating in other developmental animal models for schizophrenia, our convergent data have led us to propose that rather than all roads leading to DA, perhaps, this may be where they start

Chaotic and periodic motions of a cyclic bus induced by speedup

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