Dynamics of decision-making: from evidence accumulation to preference and belief

Decision-making is a dynamic process that begins with the accumulation of evidence and ends with the adjustment of belief. Each step is itself subject to a number of dynamic processes, such as planning, information search and evaluation. Furthermore, choice behavior reveals a number of challenging patterns, such as order effects and contextual preference reversal. Research in this field has converged toward a standard computational framework for the process of evidence integration and belief updating, based on sequential sampling models, which under some conditions are equivalent to normative Bayesian theory (Gold and Shadlen, 2007). A variety of models have been developed within the sequential sampling framework that can account for accuracy, response-time distributional data, and the speed-accuracy trade-off (Busemeyer and Townsend, 1993; Usher and Mcclelland, 2001; Brown and Heathcote, 2008; Ratcliff and McKoon, 2008). Yet there are differences between these models with regard to the mechanism of decision-termination, the optimality of the decision and the temporal weighting of the evidence. There is also a need to extend this framework to preference type of decisions (where the criteria are up to the judge) and to enrich it so as to include control processes (such as exploration/exploitation), information search, and adaptation to the environment, thereby allowing it to capture richer decision problems; for example, when alternatives are not pre-defined, or when the decision-maker is not just accumulating evidence but also adapting beliefs about the data-generating process. This Research Topic presents new work that investigates the dynamical and mathematical properties of evidence integration and its neural mechanisms and extends this framework to more complex decisions, such as those that occur during risky choice, preference formation, and belief updating. We hope these articles will encourage researchers to explore the computational and normative aspects of the decision process and the observed deviations. We briefly review here the contributions in this collection, starting from simple perceptual decisions in which the information flow is externally controlled to more complex decisions, which allow the observer to control the information flow and other learning strategies, and following on with preference formation

Developmental profile of temporal binding: from childhood to adulthood

Temporal binding refers to a phenomenon whereby the time interval between a cause and its effect is perceived as shorter than the same interval separating two unrelated events. We examined the developmental profile of this phenomenon by comparing the performance of groups of children (aged 6–7, 7–8, and 9–10 years) and adults on a novel interval estimation task. In Experiment 1, participants made judgements about the time interval between (a) their button press and a rocket launch, and (b) a non-causal predictive signal and rocket launch. In Experiment 2, an additional causal condition was included in which participants made judgements about the interval between an experimenter’s button press and the launch of a rocket. Temporal binding was demonstrated consistently and did not change in magnitude with age: estimates of delay were shorter in causal contexts for both adults and children. In addition, the magnitude of the binding effect was greater when participants themselves were the cause of an outcome compared with when they were mere spectators. This suggests that although causality underlies the binding effect, intentional action may modulate its magnitude. Again, this was true of both adults and children. Taken together, these results are the first to suggest that the binding effect is present and developmentally constant from childhood into adulthood

Senescent human melanocytes drive skin ageing via paracrine telomere dysfunction

Cellular senescence has been shown to contribute to skin ageing. However, the role of melanocytes in the process is understudied. Our data show that melanocytes are the only epidermal cell type to express the senescence marker p16(INK4A) during human skin ageing. Aged melanocytes also display additional markers of senescence such as reduced HMGB1 and dysfunctional telomeres, without detectable telomere shortening. Additionally, senescent melanocyte SASP induces telomere dysfunction in paracrine manner and limits proliferation of surrounding cells via activation of CXCR3-dependent mitochondrial ROS. Finally, senescent melanocytes impair basal keratinocyte proliferation and contribute to epidermal atrophy in vitro using 3D human epidermal equivalents. Crucially, clearance of senescent melanocytes using the senolytic drug ABT737 or treatment with mitochondria-targeted antioxidant MitoQ suppressed this effect. In conclusion, our study provides proof-of-concept evidence that senescent melanocytes affect keratinocyte function and act as drivers of human skin ageing.Pathophysiology, epidemiology and therapy of agein

Making Sense of a Sequence of Events: A Psychologically Supported AI Implementation

International audiencePeople try to make sense of the usually incomplete reports they receive about events that take place. For doing this, they make use of what they believe the normal course of thing should be. An agent's beliefs may be consonant or dissonant with what is reported. For making sense people usually ascribe different types of relations between events. A prototypical example is the ascription of causality between events. The paper proposes a systematic study of consonance and dissonance between beliefs and reports. The approach is shown to be consistent with findings in psychology. An implementation is presented with some illustrative examples

Cytoarchitectural disruption of the superior colliculus and an enlarged acoustic startle response in the Tuba1a mutant mouse

The Jenna mutant mouse harbours an S140G mutation in Tuba1a that impairs tubulin heterodimer formation resulting in defective neuronal migration during development. The consequence of decreased neuronal motility is a fractured pyramidal cell layer in the hippocampus and wave-like perturbations in the cerebral cortex. Here, we extend our characterisation of this mouse investigating the laminar architecture of the superior colliculus (SC). Our results reveal that the structure of the SC in mutant animals is intact; however, it is significantly thinner with an apparent fusion of the intermediate grey and white layers. Birthdate labelling at E12.5 and E13.5 showed that the S140G mutation impairs the radial migration of neurons in the SC. A quantitative assessment of neuronal number in adulthood reveals a massive reduction in postmitotic neurons in mutant animals, which we attribute to increased apoptotic cell death. Consistent with the role of the SC in modulating sensorimotor gating, and the circuitry that modulates this behaviour, we find that Jenna mutants exhibit an exaggerated acoustic startle response. Our results highlight the importance of Tuba1a for correct neuronal migration and implicate postnatal apoptotic cell death in the pathophysiological mechanisms underlying the tubulinopathies