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Understanding how the human brain gives rise to complex cognitive processes remains one of the biggest challenges of contemporary neuroscience. While invasive recording in animal models can provide insight into neural processes that are conserved across species, our understanding of cognition more broadly relies upon investigation of the human brain itself. There is therefore an imperative to establish non-invasive tools that allow human brain activity to be measured at high spatial and temporal resolution. In recent years, various attempts have been made to refine the coarse signal available in functional magnetic resonance imaging (fMRI), providing a means to investigate neural activity at the meso-scale, i.e. at the level of neural populations. The most widely used techniques include repetition suppression and multivariate pattern analysis. Human neuroscience can now use these techniques to investigate how representations are encoded across neural populations and transformed by relevant computations. Here, we review the physiological basis, applications and limitations of fMRI repetition suppression with a brief comparison to multivariate techniques. By doing so, we show how fMRI repetition suppression holds promise as a tool to reveal complex neural mechanisms that underlie human cognitive function. This article is part of the themed issue ‘Interpreting BOLD: a dialogue between cognitive and cellular neuroscience’.

Autism is a neurodevelopmental disorder that manifests as a heterogeneous set of social, cognitive, motor, and perceptual symptoms. This system-wide pervasiveness suggests that, rather than narrowly impacting individual systems such as affection or vision, autism may broadly alter neural computation. Here, we propose that alterations in nonlinear, canonical computations occurring throughout the brain may underlie the behavioral characteristics of autism. One such computation, called divisive normalization, balances a neuron’s net excitation with inhibition reflecting the overall activity of the neuronal population. Through neural network simulations, we investigate how alterations in divisive normalization may give rise to autism symptomatology. Our findings show that a reduction in the amount of inhibition that occurs through divisive normalization can account for perceptual consequences of autism, consistent with the hypothesis of an increased ratio of neural excitation to inhibition (E/I) in the disorder. These results thus establish a bridge between an E/I imbalance and behavioral data on autism that is currently absent. Interestingly, our findings implicate the context-dependent, neuronal milieu as a key factor in autism symptomatology, with autism reflecting a less “social” neuronal population. Through a broader discussion of perceptual data, we further examine how altered divisive normalization may contribute to a wide array of the disorder’s behavioral consequences. These analyses show how a computational framework can provide insights into the neural basis of autism and facilitate the generation of falsifiable hypotheses. A computational perspective on autism may help resolve debates within the field and aid in identifying physiological pathways to target in the treatment of the disorder. Autism is a pervasive disorder that broadly impacts perceptual, cognitive, social, and motor functioning. Across individuals, the disorder manifests with a large degree of phenotypic diversity. Here, we propose that autism symptomatology reflects alterations in neural computation. Using neural network simulations, we show that a reduction in the amount of inhibition occurring through a computation called divisive normalization can account for perceptual consequences reported in autism, as well as proposed changes in the extent to which past experience influences the interpretation of current sensory information in individuals with the disorder. A computational perspective can help bridge our understandings of the genetic/molecular basis of autism and its behavioral characteristics, providing insights into the disorder and possible courses of treatment.

Darwinian evolution tends to produce energy-efficient outcomes. On the other hand, energy limits computation, be it neural and probabilistic or digital and logical. Taking a particular energy-efficient viewpoint, we define neural computation and make use of an energy-constrained computational function. This function can be optimized over a variable that is proportional to the number of synapses per neuron. This function also implies a specific distinction between adenosine triphosphate (ATP)-consuming processes, especially computation per se vs. the communication processes of action potentials and transmitter release. Thus, to apply this mathematical function requires an energy audit with a particular partitioning of energy consumption that differs from earlier work. The audit points out that, rather than the oft-quoted 20 W of glucose available to the human brain, the fraction partitioned to cortical computation is only 0.1 W of ATP [L. Sokoloff, Handb. Physiol. Sect. I Neurophysiol. 3, 1843–1864 (1960)] and [J. Sawada, D. S. Modha, “Synapse: Scalable energy-efficient neurosynaptic computing” in Application of Concurrency to System Design (ACSD) (2013), pp. 14–15]. On the other hand, long-distance communication costs are 35-fold greater, 3.5 W. Other findings include 1) a 10⁸-fold discrepancy between biological and lowest possible values of a neuron’s computational efficiency and 2) two predictions of N, the number of synaptic transmissions needed to fire a neuron (2,500 vs. 2,000).

It has been hypothesized that the brain optimizes its capacity for computation by self-organizing to a critical point. The dynamical state of criticality is achieved by striking a balance such that activity can effectively spread through the network without overwhelming it and is commonly identified in neuronal networks by observing the behavior of cascades of network activity termed “neuronal avalanches.” The dynamic activity that occurs in neuronal networks is closely intertwined with how the elements of the network are connected and how they influence each other's functional activity. In this review, we highlight how studying criticality with a broad perspective that integrates concepts from physics, experimental and theoretical neuroscience, and computer science can provide a greater understanding of the mechanisms that drive networks to criticality and how their disruption may manifest in different disorders. First, integrating graph theory into experimental studies on criticality, as is becoming more common in theoretical and modeling studies, would provide insight into the kinds of network structures that support criticality in networks of biological neurons. Furthermore, plasticity mechanisms play a crucial role in shaping these neural structures, both in terms of homeostatic maintenance and learning. Both network structures and plasticity have been studied fairly extensively in theoretical models, but much work remains to bridge the gap between theoretical and experimental findings. Finally, information theoretical approaches can tie in more concrete evidence of a network's computational capabilities. Approaching neural dynamics with all these facets in mind has the potential to provide a greater understanding of what goes wrong in neural disorders. Criticality analysis therefore holds potential to identify disruptions to healthy dynamics, granted that robust methods and approaches are considered.

The mammalian retina engages a broad array of linear and nonlinear circuit mechanisms to convert natural scenes into retinal ganglion cell (RGC) spike outputs. Although many individual integration mechanisms are well understood, we know less about how multiple mechanisms interact to encode the complex spatial features present in natural inputs. Here, we identified key spatial features in natural scenes that shape encoding by primate parasol RGCs. Our approach identified simplifications in the spatial structure of natural scenes that minimally altered RGC spike responses. We observed that reducing natural movies into 16 linearly integrated regions described ∼80% of the structure of parasol RGC spike responses; this performance depended on the number of regions but not their precise spatial locations.We used simplified stimuli to design high-dimensional metamers that recapitulated responses to naturalistic movies. Finally, we modeled the retinal computations that convert flashed natural images into one-dimensional spike counts.

The ability to discriminate between similar sensory stimuli relies on the amount of information encoded in sensory neuronal populations. Such information can be substantially reduced by correlated trial-to-trial variability. Noise correlations have been measured across a wide range of areas in the brain, but their origin is still far from clear. Here we show analytically and with simulations that optimal computation on inputs with limited information creates patterns of noise correlations that account for a broad range of experimental observations while at same time causing information to saturate in large neural populations. With the example of a network of V1 neurons extracting orientation from a noisy image, we illustrate to our knowledge the first generative model of noise correlations that is consistent both with neurophysiology and with behavioral thresholds, without invoking suboptimal encoding or decoding or internal sources of variability such as stochastic network dynamics or cortical state fluctuations. We further show that when information is limited at the input, both suboptimal connectivity and internal fluctuations could similarly reduce the asymptotic information, but they have qualitatively different effects on correlations leading to specific experimental predictions. Our study indicates that noise at the sensory periphery could have a major effect on cortical representations in widely studied discrimination tasks. It also provides an analytical framework to understand the functional relevance of different sources of experimentally measured correlations.

Situated approaches to cognition maintain that cognition is embodied, embedded, enactive, and affective (and extended, but that is not relevant here). Situated approaches are often pitched as alternatives to computational and representational approaches, according to which cognition is computation over representations. I argue that, far from being opposites, situatedness and neural representation are more deeply intertwined than anyone suspected. To show this, I introduce a neurocomputational account of cognition that relies on neural representations. I argue not only that this account is compatible with (non-question-begging) situated approaches, but also that it requires embodiment, embeddedness, enaction, and affect at its very core. That is, constructing neural representations and their semantic content, and learning computational processes appropriate for their content, requires a tight dynamic interaction between nervous system, body, and environment. Most importantly, I argue that situatedness is needed to give a satisfactory account of neural representation: neurocognitive systems that are embodied, embedded, affective, dynamically interact with their environment, and use feedback from their interaction to shape their own representations and computations (1) can construct neural representations with original semantic content, (2) their neural vehicles and the way they are processed are automatically coordinated with their content, (3) such content is causally efficacious, (4) is determinate enough for the system’s purposes, (5) represents the distal stimulus, and (6) can misrepresent. This proposal hints at what is needed to build artifacts with some of the basic cognitive capacities possessed by neurocognitive systems.

Sensorimotor coordination is thought to rely on cerebellar-based internal models for state estimation, but the underlying neural mechanisms and specific contribution of the cerebellar components is unknown. A central aspect of any inferential process is the representation of uncertainty or conversely precision characterizing the ensuing estimates. Here, we discuss the possible contribution of inhibition to the encoding of precision of neural representations in the granular layer of the cerebellar cortex. Within this layer, Golgi cells influence excitatory granule cells, and their action is critical in shaping information transmission downstream to Purkinje cells. In this review, we equate the ensuing excitation–inhibition balance in the granular layer with the outcome of a precision-weighted inferential process, and highlight the physiological characteristics of Golgi cell inhibition that are consistent with such computations.

Nonlinear equation is an important cornerstone of nonlinear science, and many practical problems in scientific and engineering fields can be described by nonlinear equation in mathematics. In this paper, improved zeroing neural network (IZNN) models are presented and investigated for finding the solutions of the time-invariant nonlinear equation (TINE) and time-varying nonlinear equation (TVNE) in predictable and finite time. Compared with the exponential convergence zeroing neural network (ZNN), the convergence time of the IZNN models is finite and able to be estimated; in addition, the IZNN model is more stable and reliable for solving high-order TVNE. Both of the theoretical and numerical simulation results of the ZNN and IZNN for finding the solutions of the TINE and TVNE are presented to demonstrate the superiority and effectiveness of the IZNN model.

The brain is a highly diverse and heterogeneous network, yet the functional role of this neural heterogeneity remains largely unclear. Despite growing interest in neural heterogeneity, a comprehensive understanding of how it influences computation across different neural levels and learning methods is still lacking. In this work, we systematically examine the neural computation of spiking neural networks (SNNs) in three key sources of neural heterogeneity: external, network, and intrinsic heterogeneity. We evaluate their impact using three distinct learning methods, which can carry out tasks ranging from simple curve fitting to complex network reconstruction and real-world applications. Our results show that while different types of neural heterogeneity contribute in distinct ways, they consistently improve learning accuracy and robustness. These findings suggest that neural heterogeneity across multiple levels improves learning capacity and robustness of neural computation, and should be considered a core design principle in the optimization of SNNs.