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Both classic and contemporary models of auditory word repetition involve at least four left hemisphere regions: primary auditory cortex for processing sounds; pSTS (within Wernicke’s area) for processing auditory images of speech; pOp (within Broca’s area) for processing motor images of speech; and primary motor cortex for overt speech articulation. Previous functional-MRI (fMRI) studies confirm that auditory repetition activates these regions, in addition to many others. Crucially, however, contemporary models do not specify how regions interact and drive each other during auditory repetition. Here, we used dynamic causal modelling, to test the functional interplay among the four core brain regions during single auditory word and pseudoword repetition. Our analysis is grounded in the principle of degeneracy—i.e., many-to-one structure-function relationships—where multiple neural pathways can execute the same function. Contrary to expectation, we found that, for both word and pseudoword repetition, (i) the effective connectivity between pSTS and pOp was predominantly bidirectional and inhibitory; (ii) activity in the motor cortex could be driven by either pSTS or pOp; and (iii) the latter varied both within and between individuals. These results suggest that different neural pathways can support auditory speech repetition. This degeneracy may explain resilience to functional loss after brain damage.A fMRI analysis of human participants performing speech repetition tasks provides evidence for the existence of multiple, degenerate neural pathways capable of facilitating auditory repetition. [ABSTRACT FROM AUTHOR]

Active inference is a probabilistic framework for modeling the behavior of biological and artificial agents, which derives from the principle of minimizing free energy. In recent years, this framework has been applied successfully to a variety of situations where the goal was to maximize reward, often offering comparable and sometimes superior performance to alternative approaches. In this article, we clarify the connection between reward maximization and active inference by demonstrating how and when active inference agents execute actions that are optimal for maximizing reward. Precisely, we show the conditions under which active inference produces the optimal solution to the Bellman equation, a formulation that underlies several approaches to model-based reinforcement learning and control. On partially observed Markov decision processes, the standard active inference scheme can produce Bellman optimal actions for planning horizons of 1 but not beyond. In contrast, a recently developed recursive active inference scheme (sophisticated inference) can produce Bellman optimal actions on any finite temporal horizon. We append the analysis with a discussion of the broader relationship between active inference and reinforcement learning. [ABSTRACT FROM AUTHOR]

Computational models of visual attention in artificial intelligence and robotics have been inspired by the concept of a saliency map. These models account for the mutual information between the (current) visual information and its estimated causes. However, they fail to consider the circular causality between perception and action. In other words, they do not consider where to sample next, given current beliefs. Here, we reclaim salience as an active inference process that relies on two basic principles: uncertainty minimization and rhythmic scheduling. For this, we make a distinction between attention and salience. Briefly, we associate attention with precision control, i.e., the confidence with which beliefs can be updated given sampled sensory data, and salience with uncertainty minimization that underwrites the selection of future sensory data. Using this, we propose a new account of attention based on rhythmic precision-modulation and discuss its potential in robotics, providing numerical experiments that showcase its advantages for state and noise estimation, system identification and action selection for informative path planning. [ABSTRACT FROM AUTHOR]

Under the Bayesian brain hypothesis, behavioral variations can be attributed to different priors over generative model parameters. This provides a formal explanation for why individuals exhibit inconsistent behavioral preferences when confronted with similar choices. For example, greedy preferences are a consequence of confident (or precise) beliefs over certain outcomes. Here, we offer an alternative account of behavioral variability using Rényi divergences and their associated variational bounds. Rényi bounds are analogous to the variational free energy (or evidence lower bound) and can be derived under the same assumptions. Importantly, these bounds provide a formal way to establish behavioral differences through an α parameter, given fixed priors. This rests on changes in α that alter the bound (on a continuous scale), inducing different posterior estimates and consequent variations in behavior. Thus, it looks as if individuals have different priors and have reached different conclusions. More specifically, α → 0 + optimization constrains the variational posterior to be positive whenever the true posterior is positive. This leads to mass-covering variational estimates and increased variability in choice behavior. Furthermore, α → + ∞ optimization constrains the variational posterior to be zero whenever the true posterior is zero. This leads to mass-seeking variational posteriors and greedy preferences. We exemplify this formulation through simulations of the multiarmed bandit task. We note that these α parameterizations may be especially relevant (i.e., shape preferences) when the true posterior is not in the same family of distributions as the assumed (simpler) approximate density, which may be the case in many real-world scenarios. The ensuing departure from vanilla variational inference provides a potentially useful explanation for differences in behavioral preferences of biological (or artificial) agents under the assumption that the brain performs variational Bayesian inference. [ABSTRACT FROM AUTHOR]

Recent advances in neuroscience have characterised brain function using mathematical formalisms and first principles that may be usefully applied elsewhere. In this paper, we explain how active inference—a well-known description of sentient behaviour from neuroscience—can be exploited in robotics. In short, active inference leverages the processes thought to underwrite human behaviour to build effective autonomous systems. These systems show state-of-the-art performance in several robotics settings; we highlight these and explain how this framework may be used to advance robotics. [ABSTRACT FROM AUTHOR]

The active visual system comprises the visual cortices, cerebral attention networks, and oculomotor system. While fascinating in its own right, it is also an important model for sensorimotor networks in general. A prominent approach to studying this system is active inference—which assumes the brain makes use of an internal (generative) model to predict proprioceptive and visual input. This approach treats action as ensuring sensations conform to predictions (i.e., by moving the eyes) and posits that visual percepts are the consequence of updating predictions to conform to sensations. Under active inference, the challenge is to identify the form of the generative model that makes these predictions—and thus directs behavior. In this paper, we provide an overview of the generative models that the brain must employ to engage in active vision. This means specifying the processes that explain retinal cell activity and proprioceptive information from oculomotor muscle fibers. In addition to the mechanics of the eyes and retina, these processes include our choices about where to move our eyes. These decisions rest upon beliefs about salient locations, or the potential for information gain and belief-updating. A key theme of this paper is the relationship between "looking" and "seeing" under the brain's implicit generative model of the visual world. [ABSTRACT FROM AUTHOR]

Functional recovery after brain damage varies widely and depends on many factors, including lesion site and extent. When a neuronal system is damaged, recovery may occur by engaging residual (e.g., perilesional) components. When damage is extensive, recovery depends on the availability of other intact neural structures that can reproduce the same functional output (i.e., degeneracy). A system's response to damage may occur rapidly, require learning or both. Here, we simulate functional recovery from four different types of lesions, using a generative model of word repetition that comprised a default premorbid system and a less used alternative system. The synthetic lesions (i) completely disengaged the premorbid system, leaving the alternative system intact, (ii) partially damaged both premorbid and alternative systems, and (iii) limited the experience-dependent plasticity of both. The results, across 1000 trials, demonstrate that (i) a complete disconnection of the premorbid system naturally invoked the engagement of the other, (ii) incomplete damage to both systems had a much more devastating long-term effect on model performance and (iii) the effect of reducing learning capacity within each system. These findings contribute to formal frameworks for interpreting the effect of different types of lesions. [ABSTRACT FROM AUTHOR]

Active inference is a first principle account of how autonomous agents operate in dynamic, nonstationary environments. This problem is also considered in reinforcement learning, but limited work exists on comparing the two approaches on the same discrete-state environments. In this letter, we provide (1) an accessible overview of the discrete-state formulation of active inference, highlighting natural behaviors in active inference that are generally engineered in reinforcement learning, and (2) an explicit discrete-state comparison between active inference and reinforcement learning on an OpenAI gym baseline. We begin by providing a condensed overview of the active inference literature, in particular viewing the various natural behaviors of active inference agents through the lens of reinforcement learning. We show that by operating in a pure belief-based setting, active inference agents can carry out epistemic exploration—and account for uncertainty about their environment—in a Bayes-optimal fashion. Furthermore, we show that the reliance on an explicit reward signal in reinforcement learning is removed in active inference, where reward can simply be treated as another observation we have a preference over; even in the total absence of rewards, agent behaviors are learned through preference learning. We make these properties explicit by showing two scenarios in which active inference agents can infer behaviors in reward-free environments compared to both Q-learning and Bayesian model-based reinforcement learning agents and by placing zero prior preferences over rewards and learning the prior preferences over the observations corresponding to reward. We conclude by noting that this formalism can be applied to more complex settings (e.g., robotic arm movement, Atari games) if appropriate generative models can be formulated. In short, we aim to demystify the behavior of active inference agents by presenting an accessible discrete state-space and time formulation and demonstrate these behaviors in a OpenAI gym environment, alongside reinforcement learning agents. [ABSTRACT FROM AUTHOR]

Biological forms depend on a progressive specialization of pluripotent stem cells. The differentiation of these cells in their spatial and functional environment defines the organism itself; however, cellular mutations may disrupt the mutual balance between a cell and its niche, where cell proliferation and specialization are released from their autopoietic homeostasis. This induces the construction of cancer niches and maintains their survival. In this paper, we characterise cancer niche construction as a direct consequence of interactions between clusters of cancer and healthy cells. Explicitly, we evaluate these higher-order interactions between niches of cancer and healthy cells using Kikuchi approximations to the free energy. Kikuchi's free energy is measured in terms of changes to the sum of energies of baseline clusters of cells (or nodes) minus the energies of overcounted cluster intersections (and interactions of interactions, etc.). We posit that these changes in energy node clusters correspond to a long-term reduction in the complexity of the system conducive to cancer niche survival. We validate this formulation through numerical simulations of apoptosis, local cancer growth, and metastasis, and highlight its implications for a computational understanding of the etiopathology of cancer. [ABSTRACT FROM AUTHOR]

Understanding the aetiology of the diverse recovery patterns in bilingual aphasia is a theoretical challenge with implications for treatment. Loss of control over intact language networks provides a parsimonious starting point that can be tested using in-silico lesions. We simulated a complex recovery pattern (alternate antagonism and paradoxical translation) to test the hypothesis—from an established hierarchical control model—that loss of control was mediated by constraints on neuromodulatory resources. We used active (Bayesian) inference to simulate a selective loss of sensory precision; i.e., confidence in the causes of sensations. This in-silico lesion altered the precision of beliefs about task relevant states, including appropriate actions, and reproduced exactly the recovery pattern of interest. As sensory precision has been linked to acetylcholine release, these simulations endorse the conjecture that loss of neuromodulatory control can explain this atypical recovery pattern. We discuss the relevance of this finding for other recovery patterns. [ABSTRACT FROM AUTHOR]

The segregation of neural processing into distinct streams has been interpreted by some as evidence in favour of a modular view of brain function. This implies a set of specialised 'modules', each of which performs a specific kind of computation in isolation of other brain systems, before sharing the result of this operation with other modules. In light of a modern understanding of stochastic non-equilibrium systems, like the brain, a simpler and more parsimonious explanation presents itself. Formulating the evolution of a non-equilibrium steady state system in terms of its density dynamics reveals that such systems appear on average to perform a gradient ascent on their steady state density. If this steady state implies a sufficiently sparse conditional independency structure, this endorses a mean-field dynamical formulation. This decomposes the density over all states in a system into the product of marginal probabilities for those states. This factorisation lends the system a modular appearance, in the sense that we can interpret the dynamics of each factor independently. However, the argument here is that it is factorisation, as opposed to modularisation, that gives rise to the functional anatomy of the brain or, indeed, any sentient system. In the following, we briefly overview mean-field theory and its applications to stochastic dynamical systems. We then unpack the consequences of this factorisation through simple numerical simulations and highlight the implications for neuronal message passing and the computational architecture of sentience. [ABSTRACT FROM AUTHOR]