The neurobiological mechanisms of arousal and anesthesia remain poorly understood. Recent evidence highlights the key role of interactions between the cerebral cortex and the diffusely projecting matrix thalamic nuclei. Here, we interrogate these processes in a whole-brain corticothalamic neural mass model endowed with targeted and diffusely projecting thalamocortical nuclei inferred from empirical data. This model captures key features seen in propofol anesthesia, including diminished network integration, lowered state diversity, impaired susceptibility to perturbation, and decreased corticocortical coherence. Collectively, these signatures reflect a suppression of information transfer across the cerebral cortex. We recover these signatures of conscious arousal by selectively stimulating the matrix thalamus, recapitulating empirical results in macaque, as well as wake-like information processing states that reflect the thalamic modulation of largescale cortical attractor dynamics. Our results highlight the role of matrix thalamocortical projections in shaping many features of complex cortical dynamics to facilitate the unique communication states supporting conscious awareness.

Neurofeedback provides a feedback display which is linked with on-going brain activity and thus allows self-regulation of neural activity in specific brain regions associated with certain cognitive functions and is considered a promising tool for clinical interventions. Recent reviews of neurofeedback have stressed the importance of applying the “double-blind” experimental design where critically the patient is unaware of the neurofeedback treatment condition. An important question then becomes; is double-blind even possible? Or are subjects aware of the purposes of the neurofeedback experiment? – this question is related to the issue of how we assess awareness or the absence of awareness to certain information in human subjects. Fortunately, methods have been developed which employ neurofeedback implicitly, where the subject is claimed to have no awareness of experimental purposes when performing the neurofeedback. Implicit neurofeedback is intriguing and controversial because it runs counter to the first neurofeedback study, which showed a link between awareness of being in a certain brain state and control of the neurofeedback-derived brain activity. Claiming that humans are unaware of a specific type of mental content is a notoriously difficult endeavor. For instance, what was long held as wholly unconscious phenomena, such as dreams or subliminal perception, have been overturned by more sensitive measures which show that degrees of awareness can be detected. In this talk, I will discuss whether we will critically examine the claim that we can know for certain that a neurofeedback experiment was performed in an unconscious manner. I will present evidence that in certain neurofeedback experiments such as manipulations of attention, participants display residual degrees of awareness of experimental contingencies to alter their cognition.

There is growing recognition that host-associated microbiotas modulate intrinsic neurodevelopmental programs including those underlying human social behavior. Despite this awareness, the fundamental processes are generally not understood. We discovered that the zebrafish microbiota is necessary for normal social behavior. By examining neuronal correlates of behavior, we found that the microbiota restrains neurite complexity and targeting of key forebrain neurons within the social behavior circuitry. The microbiota is also necessary for both localization and molecular functions of forebrain microglia, brain-resident phagocytes that remodel neuronal arbors. In particular, the microbiota promotes expression of complement signaling pathway components important for synapse remodeling. Our work provides evidence that the microbiota modulates zebrafish social behavior by stimulating microglial remodeling of forebrain circuits during early neurodevelopment and suggests molecular pathways for therapeutic interventions during atypical neurodevelopment.

With this webinar series, the ALBA Disability & Accessibility Working Group aims to bring down the ivory tower of ableism among the brain research community, one extraordinary neuroscientist at a time. These webinars give a platform to scientists with disabilities across the globe and neuroscience disciplines, while reflecting on how to promote inclusive working environments and accessibility to research. For this 2nd episode, Prof. Philip Haydon (Tufts University School of Medicine, Boston, USA) will talk about his research and experience.  Prof. Philip runs an active laboratory researching a multitude of neurological disorders (including epilepsy). He is also President of Sail For Epilepsy. His mission is to inspire people with epilepsy, raise funds to support research for a cure, promote awareness of epilepsy and educate the public.

In popular media, there is often a connection drawn between the advent of awareness in artificial agents and those same agents simultaneously achieving human or superhuman level intelligence. In this talk, I will examine the validity and potential application of this seemingly intuitive link between consciousness and intelligence. I will do so by examining the cognitive abilities associated with three contemporary theories of conscious function: Global Workspace Theory (GWT), Information Generation Theory (IGT), and Attention Schema Theory (AST), and demonstrating that all three theories specifically relate conscious function to some aspect of domain-general intelligence in humans. With this insight, we will turn to the field of Artificial Intelligence (AI) and find that, while still far from demonstrating general intelligence, many state-of-the-art deep learning methods have begun to incorporate key aspects of each of the three functional theories. Given this apparent trend, I will use the motivating example of mental time travel in humans to propose ways in which insights from each of the three theories may be combined into a unified model. I believe that doing so can enable the development of artificial agents which are not only more generally intelligent but are also consistent with multiple current theories of conscious function.

Clinical assessment of consciousness is a significant issue, with recent research suggesting some brain-damaged patients who are assessed as unconscious are in fact conscious. Misdiagnosis of consciousness can also be detrimental when it comes to general anaesthesia, causing numerous psychological problems, including post-traumatic stress disorder. Avoiding awareness with overdose of anaesthetics, however, can also lead to cognitive impairment. Currently available objective assessment of consciousness is limited in accuracy or requires expensive equipment with major barriers to translation. In this talk, we will outline our recent theory-guided and data-driven approaches to develop new, optimized consciousness measures that will be robustly evaluated on an unprecedented breadth of high-quality neural data, recorded from the fly model system. We will overcome the subjective-choice problem in data-driven and theory-guided approaches with a comprehensive data analytic framework, which has never been applied to consciousness detection, integrating previously disconnected streams of research in consciousness detection to accelerate the translation of objective consciousness measures into clinical settings.

The purpose of this event is twofold: to raise awareness of careers in AI to neuroscience postgraduate and Early Career Researchers (ECRs), and to give the chance for commercial organisations to acquire and diversify their talent pool.  We know that our early career members are highly motivated and interested in different career pathways, and wish to help them fulfil their ambitions. This will be a hybrid event held in person at Arca Blanca, Covent Garden, London and also available online. FREE for BNA members!

Can we learn without conscious awareness? Numerous evidences in the research of implicit learning have indicated that people can learn the statistical structure of the stimuli but seemingly without any awareness of its underlying rules. However, it remains unclear what types of knowledge can be learned in implicit learning, what is the relationship between conscious and unconscious knowledge, and what are the neural substrates for the acquisition of conscious and unconscious knowledge. In this talk, I will discuss with you about these ongoing questions.

Natural perception relies inherently on inferring causal structure in the environment. However, the neural mechanisms and functional circuits that are essential for representing and updating the hidden causal structure during multisensory processing are unknown. To address this, monkeys were trained to infer the probability of a potential common source from visual and proprioceptive signals on the basis of their spatial disparity in a virtual reality system. The proprioceptive drift reported by monkeys demonstrated that they combined historical information and current multisensory signals to estimate the hidden common source and subsequently updated both the causal structure and sensory representation. Single-unit recordings in premotor and parietal cortices revealed that neural activity in premotor cortex represents the core computation of causal inference, characterizing the estimation and update of the likelihood of integrating multiple sensory inputs at a trial-by-trial level. In response to signals from premotor cortex, neural activity in parietal cortex also represents the causal structure and further dynamically updates the sensory representation to maintain consistency with the causal inference structure. Thus, our results indicate how premotor cortex integrates historical information and sensory inputs to infer hidden variables and selectively updates sensory representations in parietal cortex to support behavior. This dynamic loop of frontal-parietal interactions in the causal inference framework may provide the neural mechanism to answer long-standing questions regarding how neural circuits represent hidden structures for body-awareness and agency.

Over the past 30 years bionic devices such as cochlear implants and pacemakers, have used a small number of metal electrodes to restore function and monitor activity in patients following disease or injury of excitable tissues. Growing interest in neurotechnologies, facilitated by ventures such as BrainGate, Neuralink and the European Human Brain Project, has increased public awareness of electrotherapeutics and led to both new applications for bioelectronics and a growing demand for less invasive devices with improved performance. Coupled with the rapid miniaturisation of electronic chips, bionic devices are now being developed to diagnose and treat a wide variety of neural and muscular disorders. Of particular interest is the area of high resolution devices that require smaller, more densely packed electrodes. Due to poor integration and communication with body tissue, conventional metallic electrodes cannot meet these size and spatial requirements. We have developed a range of polymer based electronic materials including conductive hydrogels (CHs), conductive elastomers (CEs) and living electrodes (LEs). These technologies provide synergy between low impedance charge transfer, reduced stiffness and an ability to be provide a biologically active interface. A range of electrode approaches are presented spanning wearables, implantables and drug delivery devices. This talk outlines the materials development and characterisation of both in vitro properties and translational in vivo performance. The challenges for translation and commercial uptake of novel technologies will also be discussed.

Analogy offers a new interpretation of a common concern in ethics: whether decision making includes or excludes a consideration of moral issues. This is often discussed as the moral awareness of decision makers and considered a motivational concern. The possible new interpretation is that moral awareness is in part a matter of expertise. Some failures of moral awareness can then be understood as stemming from novicehood. Studies of analogical transfer are consistent with the possibility that moral awareness is in part a matter of expertise, that as a result motivation is less helpful than some prior theorizing would predict, and that many adults are not as expert in the domain of ethics as one might hope. The possibility of expert knowledge of ethical principles leads to new questions and opportunities.

Spatial neglect is a syndrome that is most frequently associated with damage to the right hemisphere, although damage to the left hemisphere can also result in signs of spatial neglect. It is characterised by absent or deficient awareness of the contralesional side of space. The screening and diagnosis of spatial neglect lacks a universal gold standard, but is usually achieved by using various modes of assessment. Spatial neglect is also difficult to treat, although prism adaptation training (PAT) has in the past reportedly showed some promise. This seminar will include highlights from a series of studies designed to identify knowledge gaps, and will suggest ways in which these can be bridged. The first study was conducted to identify and quantify clinicians’ use of assessment tools for spatial neglect, finding that several different tools are in use, but that there is an emerging consensus and appetite for harmonisation. The second study included PAT, and sought to uncover whether PAT can improve engagement in recommended therapy in order to improve the outcomes of stroke survivors with spatial neglect. The final study, a systematic review and meta-analysis, sought to investigate the scientific efficacy (rather than clinical effectiveness) of PAT, identifying several knowledge gaps in the existing literature and a need for a new approach in the study of PAT in the clinical setting.

Analogical reasoning remains foundational to the human ability to forge meaningful patterns within the sea of information that continually inundates the senses. Yet, meaningful patterns rely not only on the recognition of attributional similarities but also dissimilarities. Just as the perception of images rests on the juxtaposition of lightness and darkness, reasoning relationally requires systematic attention to both similarities and dissimilarities. With that awareness, my colleagues and I have expanded the study of relational reasoning beyond analogous reasoning and attributional similarities to highlight forms based on the nature of core dissimilarities: anomalous, antinomous, and antithetical reasoning. In this presentation, I will delineate the character of these relational reasoning forms; summarize procedures and measures used to assess them; overview key research findings; and describe how the forms of relational reasoning work together in the performance of complex problem solving. Finally, I will share critical next steps for research which has implications for instructional practice.

As Socrates said that "I know that I know nothing," our mind's function to be aware of our ignorance is essential for abstract and conceptual reasoning. However, the biological mechanism to enable such a hierarchical thought, or meta-cognition, remained unknown. In the first part of the talk, I will demonstrate our studies on the neural mechanism for metacognition on memory in macaque monkeys. In reality, awareness of ignorance is essential not only for the retrospection of the past but also for the exploration of novel unfamiliar environments for the future. However, this proactive feature of metacognition has been understated in neuroscience. In the second part of the talk, I will demonstrate our studies on the neural mechanism for prospective metacognitive matching among uncertain options prior to perceptual decision making in humans and monkeys. These studies converge to suggest that higher-order processes to self-evaluate mental state either retrospectively or prospectively are implemented in the primate neural networks.

The brain is a prediction machine. Yet the world is never entirely predictable, for any animal. Unexpected events are surprising and this typically evokes prediction error signatures in animal brains. In humans such mismatched expectations are often associated with an emotional response as well. Appropriate emotional responses are understood to be important for memory consolidation, suggesting that valence cues more generally constitute an ancient mechanism designed to potently refine and generalize internal models of the world and thereby minimize prediction errors. On the other hand, abolishing error detection and surprise entirely is probably also maladaptive, as this might undermine the very mechanism that brains use to become better prediction machines. This paradoxical view of brain functions as an ongoing tug-of-war between prediction and surprise suggests a compelling new way to study and understand the evolution of consciousness in animals. I will present approaches to studying attention and prediction in the tiny brain of the fruit fly, Drosophila melanogaster. I will discuss how an ‘active’ sleep stage (termed rapid eye movement – REM – sleep in mammals) may have evolved in the first animal brains as a mechanism for optimizing prediction in motile creatures confronted with constantly changing environments. A role for REM sleep in emotional regulation could thus be better understood as an ancient sleep function that evolved alongside selective attention to maintain an adaptive balance between prediction and surprise. This view of active sleep has some interesting implications for the evolution of subjective awareness and consciousness.

Mahzarin Banaji and her colleague coined the term “implicit bias” in the mid-1990s to refer to behavior that occurs without conscious awareness. Today, Professor Banaji is Cabot Professor of Social Ethics in the Department of Psychology at Harvard University, a member of the American Academy of Arts and Sciences, the National Academy of Sciences and has received numerous awards for her scientific contributions. The purpose of the seminar, Blindspot: Hidden Biases of Good People, is to reveal the surprising and even perplexing ways in which we make errors in assessing and evaluating others when we recruit and hire, onboard and promote, lead teams, undertake succession planning, and work on behalf of our clients or the public we serve. It is Professor Banaji’s belief that people intend well and that the inconsistency we see, between values and behavior, comes from a lack of awareness. But because implicit bias is pervasive, we must rely on scientific evidence to “outsmart” our minds. If we do so, we will be more likely to reach the life goals we have chosen for ourselves and to serve better the organizations for which we work.

My research uses a range of methods to better understand how the brain’s natural chemicals control complex behaviours, thoughts and perceptions. I also have a particular fascination about the factors that determine the contents of an individual’s conscious experience. In this talk I will present work that sits at the intersection of these two research areas looking at the role of different neurotransmitter systems in driving changes in conscious state. Specifically, I will discuss a series of studies using ambiguous stimuli to explore the neuropharmacological processes that underly alternations in perceptual awareness. By comparing different methods and neurotransmitter systems including: serotonin (psychedelics), noradrenaline (pupillometry) and Glutamate/GABA (Magnetic Resonance Spectroscopy MRS) we can start to tease apart the distinct role that different neurotransmitter systems play in coordinating conscious experience across time.

The Brain Awareness Week by the Centre for Cognitive and Brain Sciences, IIT Gandhinagar spans across 7 days and invites you for a series of talks, panel discussions, competitions and workshops on topics ranging from 'Using songbirds to understand how the brain initiates movements' to 'Cognitive Science and UX in Game Design' by speakers from prestigious Indian and International institutes. Explore the marvels of the brain by joining us on 15th March. Free Registration.

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.

Emotion processing is thought to be impaired in autism and linked to atypical visual exploration and arousal modulation to others faces and gaze, yet evidence is equivocal. We propose that, where observed, atypical socioemotional processing is due to alexithymia, a distinct but frequently co-occurring condition which affects emotional self-awareness and Interoception. In study 1 (N = 80), we tested this hypothesis by studying the spatio-temporal dynamics and entropy of eye-gaze during emotion processing tasks. Evidence from traditional and novel methods revealed that atypical eye-gaze and emotion recognition is best predicted by alexithymia in both autistic and non-autistic individuals. In Study 2 (N = 70), we assessed interoceptive and autonomic signals implicated in socioemotional processing, and found evidence for alexithymia (not autism) driven effects on gaze and arousal modulation to emotions. We also conducted two large-scale studies (N = 1300), using confirmatory factor-analytic and network modelling and found evidence that Alexithymia and Autism are distinct at both a latent level and their intercorrelations. We argue that: 1) models of socioemotional processing in autism should conceptualise difficulties as intrinsic to alexithymia, and 2) assessment of alexithymia is crucial for diagnosis and personalised interventions in autism.

Computational and cognitive neuroscience techniques have made great strides towards describing the neural computations underlying perceptual inference and decision-making under uncertainty. These tools tell us how and why perceptual illusions occur, which brain areas may represent noisy information in a probabilistic manner, and so on. However, an understanding of the subjective, qualitative aspects of perception remains elusive: qualia, or the personal, intrinsic properties of phenomenal awareness, have remained out of reach of these computational analytic insights. Here, I propose that metacognitive computations, and the subjective feelings that go along with them, give us a solid starting point for understanding subjective experience in general. Specifically, perceptual metacognition possesses ontological and practical properties that provide a powerful and unique opportunity for studying the studying the neural and computational correlates of subjective experience using established tools of computational and cognitive neuroscience. By capitalizing on decades of developments in formal computational model comparisons as applied to the specific properties of perceptual metacognition, we are now in a privileged position to reveal new and exciting insights about how the brain constructs our subjective conscious experiences.

Drug addiction is a chronically relapsing disorder characterized by compulsive drug use despite catastrophic personal consequences (e.g., loss of family, job) and even when the substance is no longer perceived as pleasurable. In this talk, I will present results of human neuroimaging studies, utilizing a multimodal approach (neuropsychology, functional magnetic resonance imaging, event-related potentials recordings), to explore the neurobiology underlying the core psychological impairments in drug addiction (impulsivity, drive/motivation, insight/awareness) as associated with its clinical symptomatology (intoxication, craving, bingeing, withdrawal). The focus of this talk is on understanding the role of the dopaminergic mesocorticolimbic circuit, and especially the prefrontal cortex, in higher-order executive dysfunction (e.g., disadvantageous decision-making such as trading a car for a couple of cocaine hits) in drug addicted individuals. The theoretical model that guides the presented research is called iRISA (Impaired Response Inhibition and Salience Attribution), postulating that abnormalities in the orbitofrontal cortex and anterior cingulate cortex, as related to dopaminergic dysfunction, contribute to the core clinical symptoms in drug addiction. Specifically, our multi-modality program of research is guided by the underlying working hypothesis that drug addicted individuals disproportionately attribute reward value to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli, with a concomitant decrease in the ability to inhibit maladaptive drug use. In this talk I will also explore whether treatment (as usual) and 6-month abstinence enhance recovery in these brain-behavior compromises in treatment seeking cocaine addicted individuals. Promising neuroimaging studies, which combine pharmacological (i.e., oral methylphenidate, or RitalinTM) and salient cognitive tasks or functional connectivity during resting-state, will be discussed as examples for using neuroimaging for empirically guiding the development of effective neurorehabilitation strategies (encompassing cognitive reappraisal and transcranial direct current stimulation) in drug addiction.