There are many mysteries in the universe. One of the most significant, often considered the final frontier in science, is understanding how our subjective experience, or consciousness, emerges from the collective action of neurons in biological systems. While substantial progress has been made over the past decades, a unified and widely accepted explanation of the neural mechanisms underpinning consciousness remains elusive. The field is rife with theories that frequently provide contradictory explanations of the phenomenon. To accelerate progress, we have adopted a new model of science: adversarial collaboration in team science. Our goal is to test theories of consciousness in an adversarial setting. Adversarial collaboration offers a unique way to bolster creativity and rigor in scientific research by merging the expertise of teams with diverse viewpoints. Ideally, we aim to harness collective intelligence, embracing various perspectives, to expedite the uncovering of scientific truths. In this talk, I will highlight the effectiveness (and challenges) of this approach using selected case studies, showcasing its potential to counter biases, challenge traditional viewpoints, and foster innovative thought. Through the joint design of experiments, teams incorporate a competitive aspect, ensuring comprehensive exploration of problems. This method underscores the importance of structured conflict and diversity in propelling scientific advancement and innovation.

Neurons in the rodent hippocampus appear to encode the position of the animal in physical space during movement. Individual ``place cells'' fire in restricted sub-regions of an environment, a feature often taken as evidence that the hippocampus encodes a map of space that subserves navigation. But these same neurons exhibit complex responses to many other variables that defy explanation by position alone, and the hippocampus is known to be more broadly critical for memory formation. Here we elaborate and test a theory of hippocampal coding which produces place cells as a general consequence of efficient memory coding. We constructed neural networks that actively exploit the correlations between memories in order to learn compressed representations of experience. Place cells readily emerged in the trained model, due to the correlations in sensory input between experiences at nearby locations. Notably, these properties were highly sensitive to the compressibility of the sensory environment, with place field size and population coding level in dynamic opposition to optimally encode the correlations between experiences. The effects of learning were also strongly biphasic: nearby locations are represented more similarly following training, while locations with intermediate similarity become increasingly decorrelated, both distance-dependent effects that scaled with the compressibility of the input features. Using virtual reality and 2-photon functional calcium imaging in head-fixed mice, we recorded the simultaneous activity of thousands of hippocampal neurons during virtual exploration to test these predictions. Varying the compressibility of sensory information in the environment produced systematic changes in place cell properties that reflected the changing input statistics, consistent with the theory. We similarly identified representational plasticity during learning, which produced a distance-dependent exchange between compression and pattern separation. These results motivate a more domain-general interpretation of hippocampal computation, one that is naturally compatible with earlier theories on the circuit's importance for episodic memory formation. Work done in collaboration with James Priestley, Lorenzo Posani, Marcus Benna, Attila Losonczy.

A complete neuroscience requires multi-level theories that address phenomena ranging from higher-level cognitive behaviors to activities within a cell. Unfortunately, we don't have cognitive models of behavior whose components can be decomposed into the neural dynamics that give rise to behavior, leaving an explanatory gap. Here, we decompose SUSTAIN, a clustering model of concept learning, into neuron-like units (SUSTAIN-d; decomposed). Instead of abstract constructs (clusters), SUSTAIN-d has a pool of neuron-like units. With millions of units, a key challenge is how to bridge from abstract constructs such as clusters to neurons, whilst retaining high-level behavior. How does the brain coordinate neural activity during learning? Inspired by algorithms that capture flocking behavior in birds, we introduce a neural flocking learning rule to coordinate units that collectively form higher-level mental constructs ("virtual clusters"), neural representations (concept, place and grid cell-like assemblies), and parallels recurrent hippocampal activity. The decomposed model shows how brain-scale neural populations coordinate to form assemblies encoding concept and spatial representations, and why many neurons are required for robust performance. Our account provides a multi-level explanation for how cognition and symbol-like representations are supported by coordinated neural assemblies formed through learning.

How and why are analogies spontaneously generated? Despite the prominence of analogy in learning and reasoning, there is little research on whether and how analogy is spontaneously generated in everyday settings. Here we fill this gap by gathering parents' answers to children's real questions, and examining analogy use in parental explanations. Study 1 found that parents used analogy spontaneously in their explanations, despite no prompt nor mention of analogy in the instruction. Study 2 found that these analogical explanations were rated highly by parents, schoolteachers, and university students alike. In Study 3, six-year-olds also rated good analogical explanations highly, but unlike their parents, did not rate them higher than causal, non-analogical explanations. We discuss what makes an analogy a good explanation, and how theories from both explanation and analogy research explain one’s motivation for spontaneously generating analogies.

The free-energy principle and active inference have received a significant attention in the fields of neuroscience and machine learning. However, it remains to be established whether active inference is an apt explanation for any given neural network that actively exchanges with its environment. To address this issue, we show that a class of canonical neural networks of rate coding models implicitly performs variational Bayesian inference under a well-known form of partially observed Markov decision process model (Isomura, Shimazaki, Friston, Commun Biol, 2022). Based on the proposed theory, we demonstrate that canonical neural networks—featuring delayed modulation of Hebbian plasticity—can perform planning and adaptive behavioural control in the Bayes optimal manner, through postdiction of their previous decisions. This scheme enables us to estimate implicit priors under which the agent’s neural network operates and identify a specific form of the generative model. The proposed equivalence is crucial for rendering brain activity explainable to better understand basic neuropsychology and psychiatric disorders. Moreover, this notion can dramatically reduce the complexity of designing self-learning neuromorphic hardware to perform various types of tasks.

Neural systems are remarkably robust against various perturbations, a phenomenon that still requires a clear explanation. Here, we graphically illustrate how neural networks can become robust. We study spiking networks that generate low-dimensional representations, and we show that the neurons’ subthreshold voltages are confined to a convex region in a lower-dimensional voltage subspace, which we call a ‘bounding box.’ Any changes in network parameters (such as number of neurons, dimensionality of inputs, firing thresholds, synaptic weights, or transmission delays) can all be understood as deformations of this bounding box. Using these insights, we show that functionality is preserved as long as perturbations do not destroy the integrity of the bounding box. We suggest that the principles underlying robustness in these networks—low-dimensional representations, heterogeneity of tuning, and precise negative feedback—may be key to understanding the robustness of neural systems at the circuit level.

Topographic maps are a prominent feature of brain organization, reflecting local and large-scale representation of the sensory surface. ​​Traditionally, such representations in early visual areas are conceived as retinotopic maps preserving ego-centric retinal spatial location while ensuring that other features of visual input are uniformly represented for every location in space. I will discuss our recent findings of a striking departure from this simple mapping in the secondary visual area (V2) of the tree shrew that is best described as a sinusoidal transformation of the visual field. This sinusoidal topography is ideal for achieving uniform coverage in an elongated area like V2 as predicted by mathematical models designed for wiring minimization, and provides a novel explanation for stripe-like patterns of intra-cortical connections and functional response properties in V2. Our findings suggest that cortical circuits flexibly implement solutions to sensory surface representation, with dramatic consequences for large-scale cortical organization. Furthermore our work challenges the framework of relatively independent encoding of location and features in the visual system, showing instead location-dependent feature sensitivity produced by specialized processing of different features in different spatial locations. In the second part of the talk, I will propose that location-dependent feature sensitivity is a fundamental organizing principle of the visual system that achieves efficient representation of positional regularities in visual input, and reflects the evolutionary selection of sensory and motor circuits to optimally represent behaviorally relevant information. The relevant papers can be found here: V2 retinotopy (Sedigh-Sarvestani et al. Neuron, 2021) Location-dependent feature sensitivity (Sedigh-Sarvestani et al. Under Review, 2022)

We use the olfactory system and forebrain of (adult) zebrafish as a model to analyze how relevant information is extracted from sensory inputs, how information is stored in memory circuits, and how sensory inputs inform behavior. A series of recent findings provides evidence that inhibition has not only homeostatic functions in neuronal circuits but makes highly specific, instructive contributions to behaviorally relevant computations in different brain regions. These observations imply that the connectivity among excitatory and inhibitory neurons exhibits essential higher-order structure that cannot be determined without dense network reconstructions. To analyze such connectivity we developed an approach referred to as “dynamical connectomics” that combines 2-photon calcium imaging of neuronal population activity with EM-based dense neuronal circuit reconstruction. In the olfactory bulb, this approach identified specific connectivity among co-tuned cohorts of excitatory and inhibitory neurons that can account for the decorrelation and normalization (“whitening”) of odor representations in this brain region. These results provide a mechanistic explanation for a fundamental neural computation that strictly requires specific network connectivity.

A myriad of pathological changes associated with epilepsy, including the loss of specific cell types, improper expression of individual ion channels, and synaptic sprouting, can be recast as decreases in cell and circuit heterogeneity. In recent experimental work, we demonstrated that biophysical diversity is a key characteristic of human cortical pyramidal cells, and past theoretical work has shown that neuronal heterogeneity improves a neural circuit’s ability to encode information. Viewed alongside the fact that seizure is an information-poor brain state, these findings motivate the hypothesis that epileptogenesis can be recontextualized as a process where reduction in cellular heterogeneity renders neural circuits less resilient to seizure onset. By comparing whole-cell patch clamp recordings from layer 5 (L5) human cortical pyramidal neurons from epileptogenic and non-epileptogenic tissue, we present the first direct experimental evidence that a significant reduction in neural heterogeneity accompanies epilepsy. We directly implement experimentally-obtained heterogeneity levels in cortical excitatory-inhibitory (E-I) stochastic spiking network models. Low heterogeneity networks display unique dynamics typified by a sudden transition into a hyper-active and synchronous state paralleling ictogenesis. Mean-field analysis reveals a distinct mathematical structure in these networks distinguished by multi-stability. Furthermore, the mathematically characterized linearizing effect of heterogeneity on input-output response functions explains the counter-intuitive experimentally observed reduction in single-cell excitability in epileptogenic neurons. This joint experimental, computational, and mathematical study showcases that decreased neuronal heterogeneity exists in epileptogenic human cortical tissue, that this difference yields dynamical changes in neural networks paralleling ictogenesis, and that there is a fundamental explanation for these dynamics based in mathematically characterized effects of heterogeneity. These interdisciplinary results provide convincing evidence that biophysical diversity imbues neural circuits with resilience to seizure and a new lens through which to view epilepsy, the most common serious neurological disorder in the world, that could reveal new targets for clinical treatment.

In the first part of this talk, I will briefly present the unfolding argument by Doerig et al. (2019) and the various replies in the philosophical and neuroscientific literature. In the second part of the talk, I will explore the ramifications that this debate has for the science of consciousness and its philosophy, with particular focus on these questions: (i) which type of explanation should a theory of consciousness provide? (ii) what is the evidential basis for theories of consciousness?

Ever since Bliss and Lømo discovered the phenomenon of long-term potentiation (LTP) in rabbit dentate gyrus in the 1960s, Hebb’s rule—neurons that fire together wire together—gained popularity to explain learning and memory. Accumulating evidence, however, suggests that neural activity is homeostatically regulated. Homeostatic mechanisms are mostly interpreted to stabilize network dynamics. However, recent theoretical work has shown that linking the activity of a neuron to its connectivity within the network provides a robust alternative implementation of Hebb’s rule, although entirely based on negative feedback. In this setting, both natural and artificial stimulation of neurons can robustly trigger network rewiring. We used computational models of plastic networks to simulate the complex temporal dynamics of network rewiring in response to external stimuli. In parallel, we performed optogenetic stimulation experiments in the mouse anterior cingulate cortex (ACC) and subsequently analyzed the temporal profile of morphological changes in the stimulated tissue. Our results suggest that the new theoretical framework combining neural activity homeostasis and structural plasticity provides a consistent explanation of our experimental observations.

Recent breakthroughs in neurobiology indicate that time is ripe to understand the cellular-level mechanisms of conscious experience. Accordingly, we have recently proposed that conscious processing depends on the integration between top-down and bottom-up information streams and that there exists a specific cellular mechanism that gates this integration. I will first describe this cellular mechanism and demonstrate how it controls signal propagation within the thalamocortical system. Then I will show how this cellular-level mechanism provides a natural explanation for why conscious experience is modulated by top-down processing. Besides shining new light on the neural basis of consciousness, this perspective unravels the mechanisms of internally generated perception, such as dreams, imagery, and hallucinations.

Sensory experience often depends on one’s own actions, including self-motion. Theories of predictive coding postulate that actions are regulated by calculating prediction error, which is the difference between sensory experience and expectation based on self-generated actions. Signals consistent with prediction error have been reported in mouse visual cortex (V1) when visual flow coupled to running was unexpectedly stopped. Here, we show such signals can be elicited by visual stimuli uncoupled to animal’s running. We recorded V1 neurons while presenting drifting gratings that unexpectedly stopped. We found strong responses to visual perturbations, which were enhanced during running. Perturbation responses were strongest in the preferred orientation of individual neurons and perturbation responsive neurons were more likely to prefer slow visual speeds. Our results indicate that prediction error signals can be explained by the convergence of known motor and sensory signals, providing a purely sensory and motor explanation for purported mismatch signals.

“Call me a marine vision scientist. Some years ago - never mind how long precisely - having little or no money in my purse, and nothing particular to interest me on shore, I thought I would sail about a little and see what animals see in the watery part of the world. It is a way I have of dividing off the spectrum, and regulating circular polarisation.” Sometimes I wish I had just set out to harpoon a white whale as it would have been easier than studying stomatopod (mantis shrimp) vision. Nowhere near as much fun of course and certainly less dangerous so in this presentation I track the history of discovery and confusion that stomatopods deliver in trying to understand what the do actually see. The talk unashamedly borrows from that of Mike Bok a few weeks ago (April 13th 2021 “The Blurry Beginnings: etc” talk) as an introduction to the system (do go look at his talk again, it is beautiful!) and goes both backwards and forwards in time, trying to provide an explanation for the design of this visual system. The journey is again one of retinal anatomy and physiology, neuroanatomy, electrophysiology, behaviour and body ornaments but this time focusses more on polarisation vision (Mike covered the colour stuff well). There is a comparative section looking at the cephalopods too and by the end, I hope you will understand where we are at with trying to understand this extraordinary way of seeing the world and why we ‘pod-people’ wave our arms around so much when asked to explain; what do stomatopods see? Maybe, to butcher another quote: “mantis shrimp have been rendered visually beautiful for vision’s sake.”

Visual knowledge obtained from our lifelong experience of the world plays a critical role in our ability to build short-term memories. We propose a mechanistic explanation of how working memory (WM) representations are built from the latent representations of visual knowledge and can then be reconstructed. The proposed model, Memory for Latent Representations (MLR), features a variational autoencoder with an architecture that corresponds broadly to the human visual system and an activation-based binding pool of neurons that binds items’ attributes to tokenized representations. The simulation results revealed that shape information for stimuli that the model was trained on, can be encoded and retrieved efficiently from latents in higher levels of the visual hierarchy. On the other hand, novel patterns that are completely outside the training set can be stored from a single exposure using only latents from early layers of the visual system. Moreover, the representation of a given stimulus can have multiple codes, representing specific visual features such as shape or color, in addition to categorical information. Finally, we validated our model by testing a series of predictions against behavioral results acquired from WM tasks. The model provides a compelling demonstration of visual knowledge yielding the formation of compact visual representation for efficient memory encoding.

I will offer a broad-brush account of what explains the emergence of agents from a physics perspective, what sorts of conditions have to be in place for them to arise, and the essential features of agents when they are viewed through the lenses of physics. One implication will be a tight link to informational asymmetries associated with the thermodynamic gradient. Another will be a reversal of the direction of explanation from the one that is usually assumed in physical discussions. In in an evolved system, while it is true in some sense that the macroscopic behavior is the way it is because of the low-level dynamics, there is another sense in which the low-level dynamics is the way that it is because of the high-level behavior it supports. (More precisely and accurately, the constraints on the configuration of its components that define system as the kind of system it is are the way they are to exploit the low-level dynamics to produce the emergent behavior.) Another will be some insight into what might make human agency special.

Comparison is a powerful learning process that improves learning in many domains. For over 10 years, my colleagues and I have researched how we can use comparison to support better learning of school mathematics within classroom settings. In 5 short-term experimental, classroom-based studies, we evaluated comparison of solution methods for supporting mathematics knowledge and tested whether prior knowledge impacted effectiveness. We next developed supplemental Algebra I curriculum and professional development for teachers to integrate Comparison and Explanation of Multiple Strategies (CEMS) in their classrooms and tested the promise of the approach when implemented by teachers in two studies. Benefits and challenges emerged in these studies. I will conclude with evidence-based guidelines for effectively supporting comparison and explanation in the classroom. Overall, this program of research illustrates how cognitive science research can guide the design of effective educational materials as well as challenges that occur when bridging from cognitive science research to classroom instruction.

The idea that behavior results from a dynamic interplay between automatic and controlled processing underlies much of decision science, but has also generated considerable controversy. In this talk, I will highlight behavioral and neural data showing how recently-developed computational models of decision making can be used to shed new light on whether, when, and how decisions result from distinct processes operating at different timescales. Across diverse domains ranging from altruism to risky choice biases and self-regulation, our work suggests that a model of prioritized attentional sampling and evidence accumulation may provide an alternative explanation for many phenomena previously interpreted as supporting dual process models of choice. However, I also show how some features of the model might be taken as support for specific aspects of dual-process models, providing a way to reconcile conflicting accounts and generating new predictions and insights along the way.

This talk will focus on different aspects of the Local Field Potential (LFP) signal. Classically, LFP fluctuations are related to changes in the functional state of the cortex. Yet, the mechanisms linking LFP changes with the state of the cortex are not well understood. The presentation will start with a brief explanation of the main oscillatory components of the LFP signal, how these different oscillatory components are generated at cortical microcircuits, and how their dynamics can be studied across multiple areas. Thereafter, a case study of a patient with akinetic mutism will be presented, linking cortical states with the behavior of the patient, as well as some preliminary results about how the LF cortical microcircuit dynamic changes modulate different cortical states and how these changes are reflected in the LFP signal

The ability to experience pain is old in evolutionary terms. It is an experience shared across species. Acute pain is the body’s alarm system, and as such it is a good thing. Pain that persists beyond normal tissue healing time (3-4 months) is defined as chronic – it is the system gone wrong and it is not a good thing. Chronic pain has recently been classified as both a symptom and disease in its own right. It is one of the largest medical health problems worldwide with one in five adults diagnosed with the condition. The brain is key to the experience of pain and pain relief. This is the place where pain emerges as a perception. So, relating specific brain measures using advanced neuroimaging to the change patients describe in their pain perception induced by peripheral or central sensitization (i.e. amplification), psychological or pharmacological mechanisms has tremendous value. Identifying where amplification or attenuation processes occur along the journey from injury to the brain (i.e. peripheral nerves, spinal cord, brainstem and brain) for an individual and relating these neural mechanisms to specific pain experiences, measures of pain relief, persistence of pain states, degree of injury and the subject's underlying genetics, has neuroscientific and potential diagnostic relevance. This is what neuroimaging has afforded – a better understanding and explanation of why someone’s pain is the way it is. We can go ‘behind the scenes’ of the subjective report to find out what key changes and mechanisms make up an individual’s particular pain experience. A key area of development has been pharmacological imaging where objective evidence of drugs reaching the target and working can be obtained. We even now understand the mechanisms of placebo analgesia – a powerful phenomenon known about for millennia. More recently, researchers have been investigating through brain imaging whether there is a pre-disposing vulnerability in brain networks towards developing chronic pain. So, advanced neuroimaging studies can powerfully aid explanation of a subject’s multidimensional pain experience, pain relief (analgesia) and even what makes them vulnerable to developing chronic pain. The application of this goes beyond the clinic and has relevance in courts of law, and other areas of society, such as in veterinary care. Relatively far less work has been directed at understanding what changes in the brain occur during altered states of consciousness induced either endogenously (e.g. sleep) or exogenously (e.g. anaesthesia). However, that situation is changing rapidly. Our recent multimodal neuroimaging work explores how anaesthetic agents produce altered states of consciousness such that perceptual experiences of pain and awareness are degraded. This is bringing us fascinating insights into the complex phenomenon of anaesthesia, consciousness and even the concept of self-hood. These topics will be discussed in my talk alongside my ‘side-story’ of life as a scientist combining academic leadership roles with doing science and raising a family.

Framing effects in individual decision-making have puzzled economists for decades because they are hard, if at all, to explain with rational choice theories. Why should mere changes in the description of a choice problem affect decision-making? Here, we examine the hypothesis that changes in framing cause changes in the allocation of attention to the different options – measured via eye-tracking – and give rise to changes in decision-making. We document that the framing of a sure alternative as a gain – as opposed to a loss – in a risk-taking task increases the attentional advantage of the sure option and induces a higher choice frequency of that option – a finding that is predicted by the attentional drift-diffusion model (aDDM). The model also correctly predicts other key findings such as that the increased attentional advantage of the sure option in the gain frame should also lead quicker decisions in this frame. In addition, the data reveal that increasing risk aversion at higher stake sizes may also be driven by attentional processes because the sure option receives significantly more attention – regardless of frame – at higher stakes. We also corroborate the causal impact of framing-induced changes of attention on choice with an additional experiment that manipulates attention exogenously. Finally, to study the precise mechanisms underlying the framing effect we structurally estimate an aDDM that allows for frame and option-dependent parameters. The estimation results indicate that – in addition to the direct effects of framing-induced changes in attention on choice – the gain frame also causes (i) an increase in the attentional discount of the gamble and (ii) an increased concavity of utility. Our findings suggest that the traditional explanation of framing effects in risky choice in terms of a more concave value function in the gain domain is seriously incomplete and that attentional mechanisms as hypothesized in the aDDM play a key role.

It is sometimes said that there are two reasons why physics is so successful as a science. One is that it deals with very simple problems. The other is that it attempts to account only for universal aspects of systems at a desired level of description, with lower level phenomena subsumed into a small number of adjustable parameters. It is a widespread belief that this approach seems unlikely to be useful in biology, which is intimidatingly complex, where “everything has an exception”, and where there are a huge number of undetermined parameters. I will try to argue, nonetheless, that there are important, experimentally-testable aspects of biology that exhibit universality, and should be amenable to being tackled from a physics perspective. My suggestion is that this can lead to useful new insights into the existence and universal characteristics of living systems. I will try to justify this point of view by contrasting the goals and practices of the field of condensed matter physics with materials science, and then by extension, the goals and practices of the newly emerging field of “Physics of Living Systems” with biology. Specific biological examples that I will discuss include the following: Universal patterns of gene expression in cell biology Universal scaling laws in ecosystems, including the species-area law, Kleiber’s law, Paradox of the Plankton Universality of the genetic code Universality of thermodynamic utilization in microbial communities Universal scaling laws in the tree of life The question of what can be learned from studying universal phenomena in biology will also be discussed. Universal phenomena, by their very nature, shed little light on detailed microscopic levels of description. Yet there is no point in seeking idiosyncratic mechanistic explanations for phenomena whose explanation is found in rather general principles, such as the central limit theorem, that every microscopic mechanism is constrained to obey. Thus, physical perspectives may be better suited to answering certain questions such as universality than traditional biological perspectives. Concomitantly, it must be recognized that the identification and understanding of universal phenomena may not be a good answer to questions that have traditionally occupied biological scientists. Lastly, I plan to talk about what is perhaps the central question of universality in biology: why does the phenomenon of life occur at all? Is it an inevitable consequence of the laws of physics or some special geochemical accident? What methodology could even begin to answer this question? I will try to explain why traditional approaches to biology do not aim to answer this question, by comparing with our understanding of superconductivity as a physical phenomenon, and with the theory of universal computation. References Nigel Goldenfeld, Tommaso Biancalani, Farshid Jafarpour. Universal biology and the statistical mechanics of early life. Phil. Trans. R. Soc. A 375, 20160341 (14 pages) (2017). Nigel Goldenfeld and Carl R. Woese. Life is Physics: evolution as a collective phenomenon far from equilibrium. Ann. Rev. Cond. Matt. Phys. 2, 375-399 (2011).

Humans spend a lifetime learning, storing and refining a repertoire of motor memories. However, it is unknown what principle underlies the way our continuous stream of sensori-motor experience is segmented into separate memories and how we adapt and use this growing repertoire. Here we develop a principled theory of motor learning based on the key insight that memory creation, updating, and expression are all controlled by a single computation – contextual inference. Unlike dominant theories of single-context learning, our repertoire-learning model accounts for key features of motor learning that had no unified explanation and predicts novel phenomena, which we confirm experimentally. These results suggest that contextual inference is the key principle underlying how a diverse set of experiences is reflected in motor behavior.

David Chalmers’s (1995) hard problem famously states: “It is widely agreed that experience arises from a physical basis, but we have no good explanation of why and how it so arises.” Thomas Nagel (1974) wrote something similar: “If we acknowledge that a physical theory of mind must account for the subjective character of experience, we must admit that no presently available conception gives us a clue about how this could be done.” This presentation will point the way towards the long-sought “good explanation” -- or at least it will provide “a clue”. I will make three points: (1) It is unfortunate that cognitive science took vision as its model example when looking for a ‘neural correlate of consciousness’ because cortical vision (like most cognitive processes) is not intrinsically conscious. There is not necessarily ‘something it is like’ to see. (2) Affective feeling, by contrast, is conscious by definition. You cannot feel something without feeling it. Moreover, affective feeling, generated in the upper brainstem, is the foundational form of consciousness: prerequisite for all the higher cognitive forms. (3) The functional mechanism of feeling explains why and how it cannot go on ‘in the dark’, free of any inner feel. Affect enables the organism to monitor deviations from its expected self-states in uncertain situations and thereby frees homeostasis from the limitations of automatism. As Nagel says, “An organism has conscious mental states if and only if there is something that it is like to be that organism—something it is like for the organism.” Affect literally constitutes the sentient subject.