Past events

Sensory stimuli in natural environments arise from many sources and the segregation of these sources into perceptually distinct objects is critical for an animal’s adaptive behavior. While segregation of visual and auditory signals has been studied extensively, little is known about the segregation of odors. I will describe our study aiming to provide a description of the behavioral ability of macrosmatic mammals to segregate odors. Specifically, we asked how the ability to segregate odors relates to features of the individual odors that are mixed. We developed a behavioral task for mice in which they were trained to report the presence of specific target odorants embedded in random background mixtures. We found that mice are highly capable of segregating an odor-figure from a background. Relating behavioral accuracy to the representations of target and background odors by olfactory receptor neurons, we found that the difficulty of segregation is not related to the similarity between odors, but rather is explained by the amount of overlap in the representations of background and target odors.

Abstract: Arm amputation provides a powerful model for studying plasticity, as it results in massive input and output loss consequential to losing a hand. Amputation also leads to profound changes in behaviour, driven by individuals’ need to compensate for severe disability (adaptive behaviour). Despite this strong behavioural pressure, research on amputation has been largely restricted to deprivation-driven (and supposedly passive) brain reorganisation, with little regard for the potential interaction between deprivation and behavioural related plasticity. As a consequence, sensory deprivation is widely held to cause maladaptive plasticity, resulting in phantom pain. Using a range of neuroimaging approaches I examine the extent to which experience modulates brain structure and function in amputees and individuals with congenital hand absence. I present evidence to challenge the proposed link between cortical reorganisation and phantom pain, and instead demonstrate preservation of topographic representations of the missing (‘phantom’) hand. I will show that phantom pain is associated with maintained representation of the phantom hand as opposed to brain plasticity, with potential implications on future treatment. Instead I provide new evidence that adaptive behaviour leads to extensive reorganisation, such that the limb engaging in compensation for disability takes over the cortical territory of the missing hand. In amputees, this process of adaptive plasticity occurs well beyond the traditionally conceptualised “critical period”. Finally, I provide new evidence for the relationship between lateralised limb-use patterns and lateralised structural and functional organisation in the resting brain. Based on this evidence, I suggest that plasticity in amputees is experience-dependant, and is not inherently maladaptive.

Abstract: Curiosity is one of the major human drives. Can we model curiosity in biological agents? Can we implement these models in artificial systems? What happens when a curious child meets a curious robot? In this talk I present recent work on the study of curiosity. First, studies of curiosity-driven behaviors in humans and rodents are presented, where we show that biological agents attempt to manage their novelty in a structured manner. A model that captures this structure is presented, wherein emergent exploration behaviors are balanced with novelty-based withdrawal-like actions. The model, which has only a few free parameters, reproduce, explain and predict many observed behaviors in mice and rats. A similar model is implemented in curious robots that learn about their own body and people interacting with them, resulting in emergent behaviors that have similar characteristics to infants’ behaviors. Finally, results from a recent study show that children’s curiosity can increase after interacting with a curious social robot. Future work on studies of infants’, children’s and adults’ curiosity-driven behavior as well as the development of autonomous curious robots, concludes the talk.

Abstract: Current information indicates that glial cells participate in most normal and pathological processes of the central nervous system. Although much less is known about satellite glial cells (SGCs) in sensory ganglia, it appears that these cells share many characteristics with their central counterparts. We found that SGCs in sensory ganglia of mice undergo major changes in a variety chronic of pain models such as axotomy, local and systemic inflammations, neuropathy induced by chemotherapeutic drugs, and diabetic neuropathy. These changes include upregulation of the glial marker glial fibrillary acidic protein (GFAP), increased cell coupling by gap junctions, and augmented responses to ATP via P2 receptors. We also showed that intercellular communications in the ganglia are mediated by calcium waves, which depend on gap junctions and P2 receptors. Our main hypothesis is that augmentation of these two factors leads to increased excitability of sensory neurons and pain. In support of this idea, blocking gap junctions reduced neuronal excitability and pain. We propose that SGCs play a major role in chronic pain and may be a suitable target for pain therapy.

Traditional models of memory dissociate memory from processes. Such tendency is rooted in the analogy between computers’ architecture and the brain, which dissociate the central processing units from the memory units. Based on such conceptualization, many empirical studies focus on simple delay periods in which memory has to be actively maintained but not processed and cases in which the integration between past and present information is undesirable. However, such models are not applicable to the majority of real life processes in which the past and present converge continuously in the processes of incoming information. Based on empirical data we outline a new framework for process-memory that resists the tendency to separate memory from process. We argue that cortical areas, ranging from early sensory areas to high order areas, has the capacity to accumulate information over time. Memory is intrinsic to each and any neural circuit, and is essential for its ability to process information. Furthermore, our data suggest that the process-memory timescale increases from early sensory areas to high order areas. Our hypothesis, that each brain area accumulates information over its preferred timescale, suggests that memories of the recent past are not stored in a few localized working memory buffers, but rather are distributed in an organized hierarchical topography throughout the nervous system. The “work of memory” is performed in virtually every neural circuit, and attentional systems modulate this ongoing processing in accordance with rule- or goal-related constraints.

One hundred sixty years after its discovery, the molecular mechanism of general anesthesia remains a notable mystery. A very wide range of agents ranging from the element xenon to steroids can act as general anesthetics on all animals from protozoa to man, suggesting that a basic cellular mechanism is involved. Electron spin resonance measurements show that volatile general anesthetics cause large changes in electron spin content of Drosophila fruit flies and that the spin responses are different in anesthesia-resistant mutants. These observations are consistent with the idea that general anesthetics perturb electron currents in cells. Electronic structure calculations on anesthetic–protein interactions are consistent with this mechanism and account for hitherto unexplained features of general anesthetic pharmacology.