Using an approach that combines experimental studies of bimanual movements to visual stimuli and theoretical modeling, the present paper develops a dynamical account of sensorimotor learning, that is, how new skills are acquired and old ones modified. A significant aspect of our approach is the focus on the individual learner as the basic unit of analysis, in particular the quantification of predispositions and capabilities that the individual learner brings to the learning environment. Such predispositions constitute the learner's behavioral repertoire, captured here theoretically as a dynamical landscape (“intrinsic dynamics”). The learning process is demonstrated to not only lead to a relatively permanent improvement of performance in the required task—the usual outcome—but also to alter the individual's entire repertoire. Changes in the dynamical landscape due to learning are shown to result from two basic mechanisms or “routes”: bifurcation and shift. Which mechanism is selected depends the initial individual repertoire before new learning begins. Both bifurcation and shift mechanisms are accommodated by a dynamical model, a relatively straightforward development of the well-established HKB model of movement coordination. Model simulations show that although environmental or task demands may be met equally well using either mechanism, the bifurcation route results in greater stabilization of the to-be-learned behavior. Thus, stability not (or not only) error is demonstrated to be the basis of selection, both of a new pattern of behavior and the path (smooth shift versus abrupt qualitative change) that learning takes. In line with these results, recent neurophysiological evidence indicates that stability is a relevant feature around which brain activity is organized while an individual performs a coordination task. Finally, we explore the consequences of the dynamical approach to learning for theories of biological change.

Humans’ interactions with each other or with socially competent machines exhibit lawful coordination patterns at multiple levels of description. According to Coordination Dynamics, such laws specify the flow of coordination states produced by functional synergies of elements (e.g., cells, body parts, brain areas, people…) that are temporarily organized as single, coherent units. These coordinative structures or synergies may be mathematically characterized as informationally coupled self-organizing dynamical systems (Coordination Dynamics). In this paper, we start from a simple foundation, an elemental model system for social interactions, whose behavior has been captured in the Haken-Kelso-Bunz (HKB) model. We follow a tried and tested scientific method that tightly interweaves experimental neurobehavioral studies and mathematical models. We use this method to further develop a body of empirical research that advances the theory toward more generalized forms. In concordance with this interdisciplinary spirit, the present paper is written both as an overview of relevant advances and as an introduction to its mathematical underpinnings. We demonstrate HKB’s evolution in the context of social coordination along several directions, with its applicability growing to increasingly complex scenarios. In particular, we show that accommodating for symmetry breaking in intrinsic dynamics and coupling, multiscale generalization and adaptation are principal evolutions. We conclude that a general framework for social coordination dynamics is on the horizon, in which models support experiments with hypothesis generation and mechanistic insights.

Coordination is a ubiquitous feature of all living things. It occurs by virtue of informational coupling among component parts and processes and can be quite specific (as when cells in the brain resonate to signals in the environment) or nonspecific (as when simple diffusion creates a source–sink dynamic for gene networks). Existing theoretical models of coordination—from bacteria to brains to social groups—typically focus on systems with very large numbers of elements (N→∞) or systems with only a few elements coupled together (typically N = 2). Though sharing a common inspiration in Nature’s propensity to generate dynamic patterns, both approaches have proceeded largely independent of each other. Ideally, one would like a theory that applies to phenomena observed on all scales. Recent experimental research by Mengsen Zhang and colleagues on intermediate-sized ensembles (in between the few and the many) proves to be the key to uniting large- and small-scale theories of coordination. Disorder–order transitions, multistability, order–order phase transitions, and especially metastability are shown to figure prominently on multiple levels of description, suggestive of a basic Coordination Dynamics that operates on all scales. This unified coordination dynamics turns out to be a marriage of two well-known models of large- and small-scale coordination: the former based on statistical mechanics (Kuramoto) and the latter based on the concepts of Synergetics and nonlinear dynamics (extended Haken–Kelso–Bunz or HKB). We show that models of the many and the few, previously quite unconnected, are thereby unified in a single formulation. The research has led to novel topological methods to handle the higher-dimensional dynamics of coordination in complex systems and has implications not only for understanding coordination but also for the design of (biorhythm inspired) computers.

In this paper we demonstrate that retrograde signaling via astrocytes may underpin self-repair in the brain. Faults manifest themselves in silent or near silent neurons caused by low transmission probability synapses; the enhancement of the transmission probability of a healthy neighbouring synapse by retrograde signaling can enhance the transmission probability of the “faulty” synapse (repair). Our model of self-repair is based on recent research showing that retrograde signaling via astrocytes can increase the probability of neurotransmitter release at damaged or low transmission probability synapses. The model demonstrates that astrocytes are capable of bidirectional communication with neurons which leads to modulation of synaptic activity, and that indirect signaling through retrograde messengers such as endocannabinoids leads to modulation of synaptic transmission probability. Although our model operates at the level of cells, it provides a new research direction on brain-like self-repair which can be extended to networks of astrocytes and neurons. It also provides a biologically inspired basis for developing highly adaptive, distributed computing systems that can, at fine levels of granularity, fault detect, diagnose and self-repair autonomously, without the traditional constraint of a central fault detect/repair unit.