Seminars

Organisms face challenges to survival throughout life. When we freeze or flee in danger, we often feel fear. Tracing the deep history of danger gives a different perspective. The first cells living billions of years ago had to detect and respond to danger in order to survive. Life is about not being dead, and behavior is a major way that organisms hold death off. Although behavior does not require a nervous system, complex organisms have brain circuits for detecting and responding to danger, the deep roots of which go back to the first cells. But these circuits do not make fear, and fear is not the cause of why we freeze or flee. Fear a human invention; a construct we use to account for what happens in our minds when we become aware that we are in harm’s way. This requires a brain that can personally know that it existed in the past, that it is the entity that might be harmed in the present, and that it will cease to exist it the future. If other animals have conscious experiences, they cannot have the kinds of conscious experiences we have because they do not have the kinds of brains we have. This is not meant as a denial of animal consciousness; it is simply a statement about the fact that every species has a different brain. Nor is it a declaration about the wonders of the human brain, since we have done some wonderful, but also horrific, things with our brains. In fact, we are on the way to a climatic disaster that will not, as some suggest, destroy the Earth. But it will make it inhabitable for our kind, and other organisms with high energy demands. Bacteria have made it for billions of years and will likely be fine. The rest is up for grabs, and, in a very real sense, up to us.

Research, whether direct or indirect, aims to advance knowledge and change the world for the better. But whether you are spike-sorting with high-performance computers, getting through 100 single-use plastic pipette tips in a day or receiving regular shipments of metal-rich equipment, your research is having a long-term and detrimental impact on the environment. This session will explore how life sciences research contributes to the climate crisis and negatively impacts local and global environments. Practical advice will be given on ways to reduce the footprint of your own research.

In Europe, the number of people aged 65 and older is increasing dramatically, and research related to ageing is more crucial than ever. The main research dedicated to age-related changes concentrates on cognitive or sensory deficits. This is also the case in vision research. However, the majority of older adults ages without major cognitive or optical or deficits. These are foremost good news, but even in the absence of neurodegenerative or eye diseases changes in visual perception occur. It has been suggested that age-related changes are due to a general decline of cognitive, perceptual and sensory functions. However, more recent studies reveal large individual differences within the ageing population and whereas some functions show age-related deterioration, others are surprisingly unaffected. Overall, it becomes increasingly apparent that perceptual changes in healthy ageing cannot be attributed to one single underlying factor. I will present studies from various areas of visual perception that challenge the view that age-related changes are primarily related to decline. Instead, our findings suggest that age-related changes are the result of visual experience, such that the brain ages optimally given the input it receives.

In order to successfully navigate through the environment, animals must accurately estimate the status of their motion with respect to the surrounding scene and objects. In this talk, I will present our recent work on how retrosplenial cortical (RSC) neurons combine vestibular and visual signals to reliably encode the direction and speed of head turns during passive motion and active navigation. I will discuss these data in the context of RSC long-range connectivity and further show our ongoing work on building population-level models of motion representation across cortical and subcortical networks.

For many animals, the sense of olfaction plays a major role in controlling sexual behaviors. Olfaction helps animals to detect mates, discriminate their status, and ultimately, decide on their behavioral output such as courtship behavior or aggression. Specific pheromone cues and receptors have provided a useful model to study how sensory inputs are converted into certain behavioral outputs. With the aid of recent advances in tools to record and manipulate genetically defined neurons, our understanding of the neural basis of sexual and social behavior has expanded substantially. I will discuss the current understanding of the neural processing of sex pheromones and the neural circuitry which controls sexual and social behaviors and ultimately reproduction, by focusing on rodent studies, mainly in mice, and the vomeronasal sensory system.

Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. While human insular cortex (InsCtx) is implicated in interoception, the cellular and circuit mechanisms remain unclear. I will describe our recent work imaging mouse InsCtx neurons during two physiological deficiency states – hunger and thirst. InsCtx ongoing activity patterns reliably tracked the gradual return to homeostasis, but not changes in behavior. Accordingly, while artificial induction of hunger/thirst in sated mice via activation of specific hypothalamic neurons (AgRP/SFOGLUT) restored cue-evoked food/water-seeking, InsCtx ongoing activity continued to reflect physiological satiety. During natural hunger/thirst, food/water cues rapidly and transiently shifted InsCtx population activity to the future satiety-related pattern. During artificial hunger/thirst, food/water cues further shifted activity beyond the current satiety-related pattern. Together with circuit-mapping experiments, these findings suggest that InsCtx integrates visceral-sensory inputs regarding current physiological state with hypothalamus-gated amygdala inputs signaling upcoming ingestion of food/water, to compute a prediction of future physiological state.

Transient changes in dopamine activity in response to reward and punishment have been known to regulate reward-related learning. However, the cellular basis that detects the transient dopamine signaling has long been unclear. Using two-photon microscopy and optogenetics, I have shown that transient increases and decreases of dopamine modulate plasticity of dopamine D1 and D2 receptor-expressing cells in the nucleus accumbens, respectively. At the behavioral level, I characterized that these D1 and D2 cells cooperatively tune learning by generalization and discrimination learning. Interestingly, disturbance of the dopamine signaling impaired D2 cell plasticity and discrimination learning, which was analogous to salience misattribution seen in subjects with schizophrenia.

The last decade in the field of neuroscience has been marked by intense debate on the meaning of the term fear. Whereas some have argued that fear (as well as other emotions) relies on cognitive capacities that are unique to humans, others view it as a negative state constructed from essential building blocks. This latter definition posits that fear states are associated with varying readouts that one could consider to be parallel processes or serial events tied to a specific hierarchy. Within this framework, innate defensive behaviors are considered to be common displays of fear states that lie under the control of hard-wired brain circuits. As a general rule, these defensive behaviors can be classified as either reactive or cognitive based on a thread imminence continuum. However, while evidence of the neuronal circuits that lead to these divergent behavioral strategies has accrued over the last decades, most literature has considered these responses in isolation. As a result, important misconceptions have arisen regarding how fear circuits are distributed in the brain and the contribution of specific nodes within these circuits to defensive behaviors. To mitigate the status quo, I will conduct a systematic comparison of brain circuits driving the expression of freezing and active avoidance behavior, which I will use as well-studied proxies of reactive and cognitive fear, respectively. In addition, I propose that by integrating associative information with interoceptive and exteroceptive signals the central nucleus of the amygdala plays a crucial role in biasing the selection of defensive behaviors.

There is a surprising consistency in the images we remember and forget – across observers, certain images are intrinsically more memorable than others in spite of our diverse individual experiences. The perception of images at different memorability levels also results in stereotyped patterns in visual and mnemonic regions in the brain, regardless of an individual’s actual memory for that item. In this talk, Dr. Bainbridge will discuss our current neuroscientific understanding of how memorability is represented in patterns in the brain, potentially serving as a signal for how stimulus information is prioritized for eventual memory encoding.

This talk will focus on two areas. I will firstly discuss some new data, starting with insights from rare human genetic variants, which helps to clarify the role of the central melanocortin system in the acquisition of nutrients and their disposition into growth, the acquisition of lean mass and sexual maturation . I will then discuss some aspects of the emerging biology of GDF15; a sentinel hormone conveying information regarding a range of somatic stresses to the brain.

Eyes abound in the animal kingdom. Some are large as basketballs and others are just fractions of a millimetre. Eyes also come in many different types, such as the compound eyes of insects, the mirror eyes of scallopsor our own camera-like eyes. Common to all animal eyes is that they serve the same fundamental role of collecting external information for guidingthe animal’s behaviour. But behaviours vary tremendously across the animal kingdom, and it turns outthis is the key to understand how eyes evolved. The lecture will take a tour from the first animals that could only sense the presence of light, to those that saw the first crude image of the world and finally to animals that use acute vision for interacting with otheranimals. Amazingly, all these stages of eye evolution still exist in animals living today, and this is how we can unravel the evolution of behaviours that has been the driving force behind eye evolution

Adult hippocampal neurogenesis is implicated in memory formation and mood regulation. The Thuret lab investigates environmental and molecular mechanisms controlling the production of these adult-born neurons and how they impact mental health. We study neurogenesis in healthy ageing as well as in the context of diseases such as Alzheimer’s and depression. By approaching neurogenesis in health and disease, the strategy is two folds: (i) Validating the neurogenic process as a target for prevention and pharmacological interventions. (ii) Developing neurogenesis as a biomarker of disease prediction and progression. In this talk, I will focus on presenting some recent human studies demonstrating how hippocampal neural stem cells fate can be used as biomarkers of cognitive aging and dementia.

Open-source tools are gaining an increasing foothold in neuroscience. The rising complexity of experiments in systems neuroscience has led to a need for multiple parts of experiments to work together seamlessly. This means that open-source tools that freely interact with each other and can be understood and modified more easily allow scientists to conduct better experiments with less effort than closed tools. Open Ephys is an organization with team members distributed all around the world. Our mission is to advance our understanding of the brain by promoting community ownership of the tools we use to study it. We are making and distributing cutting edge tools that exploit modern technology to bring down the price and complexity of neuroscience experiments. A large component of this is to take tools that were developed in academic labs and helping with documentation, support, and distribution. More recently, we have been working on bringing high-quality manufacturing, distribution, warranty, and support to open source tools by partnering with OEPS in Portugal. We are now also establishing standards that make it possible to combine methods, such as miniaturized microscopes, electrode drive implants, and silicon probes seamlessly in one system. In the longer term, our development of new tools, interfaces and our standardization efforts have the goal of making it possible for scientists to easily run complex experiments that span from complex behaviors and tasks, multiple recording modalities, to easy access to data processing pipelines.

Integrated information theory (IIT) takes as its starting point phenomenology, rather than behavioral, functional, or neural correlates of consciousness. The theory characterizes the essential properties of phenomenal existence—which is immediate and indubitable. These are translated into physical properties, expressed operationally as cause-effect power, which must be satisfied by the neural substrate of consciousness. On this basis, the theory can account for clinical and experimental data about the presence and absence of consciousness. Current work aims at accounting for specific qualities of different experiences, such as spatial extendedness and the flow of time. Several implications of IIT have ethical relevance. One is that functional equivalence does not imply phenomenal equivalence—computers may one day be able to do everything we do, but they will not experience anything. Another is that we do have free will in the fundamental, metaphysical sense—we have true alternatives and we, not our neurons, are the true cause of our willed actions.

Agent-causal libertarian free will asserts that the conscious agent is the ultimate cause of her own voluntary behavior. A major reason to reject libertarian free will is that it seems incompatible with our current knowledge of physics. In this talk I will argue how quantum processes, specifically non-random collapses of the wavefunction in the human cortex, may enable libertarian free will. I will discuss how this account can be empirically tested.