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December
3rd
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Monday, December 03
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Opening remarks
Sergio T. Ferreira (Chair, Program in Basic and Clinical Neuroscience)
Aβ oligomers and inflammation link Alzheimer’s disease and depression
Depression is one of the most common psychiatric symptoms in Alzheimer’s disease (AD), and considerable evidence indicates that major depressive disorder increases the risk of AD. To date, however, the molecular mechanisms underlying the clinical association between depression and AD have remained elusive. Soluble oligomers of the amyloid-b peptide (AbOs) accumulate in the brains of AD patients and are increasingly recognized as the proximal neurotoxins responsible for synapse failure and memory deficits in AD. We have hypothesized that AbOs might be mechanistically linked to behavioral changes in AD. In order to test this hypothesis, mice were given a single intracerebroventricular (i.c.v.) injection of 10 pmol AβOs and were subsequently evaluated in tests aimed to detect depressive-like behavior. Surprisingly, compared to vehicle-injected control mice, AβO-injected mice exhibited significantly increased immobility in the Porsolt forced swim test and in the tail suspension test. AbO-injected mice further exhibited anhedonic behavior revealed by the sucrose preference test. I.c.v. injection of AbOs also caused cognitive deficits revealed by the novel object recognition test. Interestingly, the antidepressant fluoxetine rescued both depressive-like behavior and cognitive deficit in AbO-injected mice. Behavioral and cognitive alterations induced by AbOs correlated with an inflammatory process, with increased cytokine levels and recruitment of microglia and astrocytes in the mouse brain. The current findings establish that AbOs link memory impairment and depressive-like behavior in mice, providing molecular mechanistic support to clinical evidence connecting AD and depressive disorder. By revealing that AbOs underlie both cognitive and depressive-like symptoms in mice, our results suggest a mechanism by which elevated brain levels of AbOs may be linked to changes in cognition and mood in AD.
Roberto Lent (Director, Institute of Biomedical Sciences, Federal University of Rio de Janeiro)
The Human Brain In Numbers: From Ancient Ages To Old Ages
Due to methodological shortcomings and a certain conservatism that consolidates wrong assumptions in the literature, some dogmas became established and reproduced in papers and textbooks, derived from quantitative features of the brain. The first dogma states that the cerebral cortex is the pinnacle of brain evolution – based on the observations that its volume is greater in more “intelligent” species, and that cortical surface area grows more than any other brain region, to reach the largest proportion in higher primates and humans. The second dogma claims that the human brain would contain 100 billion neurons, plus 10-fold more glial cells. These round numbers became largely adopted, although data provided by different authors led to a broad discrepancy range of 75-125 billion neurons in the whole brain. The third dogma derives from the second, and states that our brain is structurally special, an outlier as compared with other primates. Being so large and convoluted, it would be a special construct of nature, unrelated from evolutionary scaling. Finally, the fourth dogma appeared as a tentative explanation for the considerable growth of the brain along development and evolution: being modular in structure, the brain (and particularly the cerebral cortex) would grow by tangential addition of modules uniform in neuronal composition. In this lecture, we intend to examine and challenge these four dogmas, propose other interpretations or simply their substitution by alternative views, and in addition present recent data on sexual dimorphism and the effects of ageing in the absolute cellular composition of the human brain.
The recent epidemic of obesity threatens not only the health and longevity of those directly affected, but will also cripple economies as health care costs skyrocket and productivity declines. Particularly troubling is the evidence that sedentary and gluttonous lifestyles compromise the performance of the brain and increase the risk for Alzheimer’s disease (AD), Parkinson’s disease (PD) and stroke. Our research has elucidated the cellular and molecular mechanisms responsible for the adverse effects of high energy diets and lack of exercise on brain function and vulnerability to AD, PD and stroke (Mattson MP. Cell Metabolism, in press). On the other hand, dietary energy restriction, particularly intermittent energy restriction/fasting (IER), can protect neurons against dysfunction and degeneration in experimental models of AD, PD and stroke. Energy restriction and exercise activate adaptive cellular stress response signaling pathways in neurons resulting in the production of neurotrophic factors, protein chaperones, DNA repair enzymes and proteins critical for mitochondrial biogenesis. Among these factors, brain-derived neurotrophic factor (BDNF) appears to be particularly important in enhancing synaptic plasticity, neurogenesis and cognitive performance. Excessive energy intake, particularly in combination with a sedentary lifestyle reduces the activation of adaptive cellular stress response pathways thereby rendering neurons vulnerable to dysfunction and degeneration. Our societies are therefore faced with a major challenge: implement IER- and exercise-based prescriptions for brain health beginning in young adulthood NOW, or endure a continuing epidemic of poor brain health and neurodegenerative disorders for the foreseeable future.
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Cocktail and get together
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December 4th
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Session 1: Brain development and senescence
Suzana Herculano-Houzel (Inst. Biomedical Sciences, Federal Univ. of Rio de Janeiro, Brazil)
How to build a bigger brain: Pre-natal and post-natal mechanisms lead to varying brain size in rodents
What are the developmental mechanisms that lead to diversity in brain size and the numbers of cells that compose them? We have recently shown that while the relationship between the size of brain structures and their numbers of non-neuronal cells is shared across structures, species and mammalian orders, the relationship between brain structure size and numbers of neuronal cells is diverse. This implies that while non-neuronal cells are added in similar fashion to developing brain structures regardless of their identity and species, the rules governing the addition of neurons during development is structure- and order-specific.
In this talk I will compare how numbers of neuronal and non-neuronal cells are added to the brain of two rodent species, the laboratory mouse and rat. Mammalian brain neurons have been traditionally considered to be born prenatally, with the exception of the cerebellum. Postnatal brain growth therefore is usually explained simply by an increase of the neuronal cell size and by the addition of glial cells. However, both mouse and rat gain large numbers of neurons in the cerebral cortex and in the ensemble of brainstem and diencephalon in the first postnatal week of life, such that the numbers of neurons in these structures nearly doubles within the period. Next, both species lose large numbers of neurons throughout the brain (except in the cerebellum), while non-neuronal cells are added in large numbers. Comparison of the developmental timelines shows that the difference in adult numbers of neurons across the two species are related to both prenatal and postnatal mechanisms affecting the addition of neurons and their average cell size, without significant differences in how non-neuronal cells are added. These findings have direct implications for the understanding of the developmental mechanisms that lead to the evolution of brain size in mammals.
Stephen C. Noctor (Dept. Psychiatry and Behavioral Sciences, UC Davis MIND Institute, USA)
Regulation of prenatal cortical neurogenesis
The mammalian cerebralcortex arises from precursor cells that reside in a proliferative regionsurrounding the lateral ventricles of the developing brain. Recent work hasshown that precursor cells in the subventricular zone (SVZ) provide a majorcontribution to prenatal cortical neurogenesis, and that the SVZ issignificantly thicker in gyrencephalic mammals than it is in lissencephalicmammals. Comparing the characteristics of cortical precursor cells acrossspecies may shed light on factors that regulate cortical neurogenesis and maypoint toward mechanisms that underlie the evolutionary expansion of theneocortex in primates. We analyzed the characteristics of Pax6+ and Tbr2+precursor cells in the cerebral cortex of gyrencephalic macaques and ferrets,and lissencephalic rats, paying special attention to the SVZ. The distributionof these neural precursor cells did not correlate with gyrencephaly, butinstead was more similar in lissencephalic rats and gyrencephalic ferrets, thanin the gyrencephalic cortex of macaque. Furthermore, we found that thecytoarchitectural features and cell types that define the outer SVZ in primatesare also present in the developing rat neocortex. Finally we examined how the numberof neural precursor cells is regulated during neurogenic phases of corticaldevelopment. We found that glial cells interact with neural precursor cells ina manner that regulates the size of the neural precursor cell pool in bothprimates and rodents. We also found evidence that these interactions arepresent in the developing reptilian brain, suggesting that this mechanism forregulating cell number has been a constant feature throughout evolution.
Coffee break
Michael Merzenich (Coleman Memorial Lab., Univ. of California at San Francisco, USA)
Brain Plasticity-Based Therapeutics
Roberto Lent (Inst. Biomedical Sciences, Federal Univ. of Rio de Janeiro, Brazil)
The human brain in numbers: From ancient ages to old ages
Due to methodological shortcomings and a certain conservatism that consolidates wrong assumptions in the literature, some dogmas became established and reproduced in papers and textbooks, derived from quantitative features of the brain. The first dogma states that the cerebral cortex is the pinnacle of brain evolution – based on the observations that its volume is greater in more “intelligent” species, and that cortical surface area grows more than any other brain region, to reach the largest proportion in higher primates and humans. The second dogma claims that the human brain would contain 100 billion neurons, plus 10-fold more glial cells. These round numbers became largely adopted, although data provided by different authors led to a broad discrepancy range of 75-125 billion neurons in the whole brain. The third dogma derives from the second, and states that our brain is structurally special, an outlier as compared with other primates. Being so large and convoluted, it would be a special construct of nature, unrelated from evolutionary scaling. Finally, the fourth dogma appeared as a tentative explanation for the considerable growth of the brain along development and evolution: being modular in structure, the brain (and particularly the cerebral cortex) would grow by tangential addition of modules uniform in neuronal composition. In this lecture, we intend to examine and challenge these four dogmas, propose other interpretations or simply their substitution by alternative views, and in addition present recent data on sexual dimorphism and the effects of ageing in the absolute cellular composition of the human brain.
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Eat and meet time
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Session 2: Imaging brain plasticity and higher functions
Fernanda Tovar-Moll (Inst. Biomedical Sciences, Federal Univ. of Rio de Janeiro & IDOR Institute, Brazil)
Short- and Long-distance Plasticity: Functional and Morphological Evidence
Although a lot has been learned on the function of specific brain structures, we still know very little about how different structures are interrelated, leading to the emergence of complex functions. Novel imaging techniques have opened new windows for the investigation of changes in brain networks in normal and pathological conditions. In addition, several studies using these advanced techniques have provided important evidence on the brain capacity to reorganize after environmental influences. Combining functional and structural magnetic resonance imaging and electrophysiological techniques, we will present evidence of this striking capacity of structural and functional reorganization. This will be illustrated by the formation of grossly anomalous long projection-white-matter tracts during abnormal development, as well as by the changes in cortical and white matter circuits in the adult brain in response to environmental challenges.
Linda J. Richards (Queensland Brain Institute, Univ. of Queensland, Australia)
The development and evolution of commissural projections in the nervous system
Across all species of animals with a bilaterally symmetrical body plan, the development of the nervous system is characterized by both ipsilaterally projecting and contralaterally projecting neurons. The distinction between these two populations of neurons occurs at the midline where developing axons are guided to either grow across the midline or to remain ipsilateral. Thus, the midline of the developing nervous system is an area where axonal guidance molecules have been identified that direct this choice and provide critical guidance cues for contralaterally projecting axons known as commissural axons.
There are many important commissural projections in the brain and spinal cord of both vertebrates and invertebrates. One characteristic that is highly conserved across all species and all commissures, is the presence of midline glial structures that express axonal guidance cues to regulate commissural axon guidance. The molecules expressed by these glia are also highly conserved, with homologous molecules conserved from flies to humans. The presence of commissural projections occurs primarily in the central nervous system of animals and thus the evolution of commissural projections has been studied in the brain and spinal cord. Another feature of commissural projections throughout evolution is that additional commissural projections have been “added” as the brain has become more complex. The evolutionarily most recent commissural projection in the human brain is the corpus callosum, which is the largest of all commissural projections.
The formation of commissural projections in the developing brain is regulated by a number of different developmental mechanisms. These include the formation of the commissural plate, the guidance of commissural axons by midline glial populations, and the expression of specific axon guidance molecules. There are three commissural projections in the telencephalon; the corpus callosum, the hippocampal commissure and the anterior commissure, all of which function to integrate information from the two telencephalic hemispheres. Recent data from our laboratory indicates that the correct patterning and formation of the commissural plate provides an essential substrate for commissure formation in the telencephalon. In addition to this function, the commissural plate expresses members of the fibroblast growth factor family of molecules, which we have recently found to act as guidance molecules for telencephalic commissural axons. Our work utilizes diffusion imaging and MRI-based tractography coupled with molecular and anatomical tract tracing methods to discover the fundamental mechanisms that regulate brain wiring.
Coffee break
Roland Zahn (School of Psychological Sciences, Univ. of Manchester, UK)
Translational cognitive neuroscience of social knowledge and moral motivations: new clues for the understanding of affective disorders
There is a widespread recognition that neuropsychiatric disorders such as major depressive disorder (MDD) cannot be understood without identifying the cognitive and anatomical components underpinning socio-moral cognition and emotion. Despite the current flourishing of social cognitive neuroscience, bridging the gap between the phenomenology of distinctive neuropsychiatric symptoms and their cognitive neuroanatomy remains difficult. This talk builds on our earlier fMRI and patient lesion mapping evidence supporting the importance of the right superior anterior temporal lobe (ATL) in representing social conceptual knowledge (enabling us to understand e.g. “stingy”, or “polite” qualities of social behaviour). In keeping with predictions of a temporo-fronto-subcortical integration model of moral cognition and emotion, we found the right superior ATL to dynamically change its network of functional connections depending on the context of moral feeling (including the septal-subgenual region for guilt and lateral orbitofrontal cortex for indignation). Septal-subgenual activation was associated with the experience of guilt in healthy participants. Interestingly, the septal-subgenual region is known to display abnormal metabolism in major depressive disorder (MDD) when symptomatic. Despite the theoretical importance of guilt and self-blame, first highlighted by Freud, its neural basis in MDD was unknown. A recent fMRI study addressed this question comparing people with MDD fully remitted from symptoms with a control group with no history of MDD. As predicted, overgeneralised self-blame and MDD were associated with functional disconnection between the right superior ATL and septal-subgenual cingulate region when patients with MDD experienced guilt but not whilst experiencing indignation. Future translational research directions will be discussed.
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December 5th
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Wednesday, December 05
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Session 4: The diseased brain: prions and Alzheimer’s disease
David Westaway (Center for Prions and Protein Folding Diseases, Univ. Alberta, Canada)
Locking-Down Prion Infections
Prion diseases exhibit accumulation of PrPSc, a misfolded form of the C-terminal region of the cellular protein PrPC, and an apparently synchronous disappearance of the PrPC-like Shadoo (Sho) protein. Aside from a role in prion infections, PrPC is also notorious as a binding partner for oligomeric preparations of Alzheimer’s Disease (AD) Ab peptide. For Sho we have a) tested the hypothesis that Sho can influence prion disease pathogenesis, as suggested by human molecular genetic studies, by constructing Sprn0/0 knockout mice1 and challenging them by prion infection, and b) assessed the molecular basis of down-regulation in prion infections using a novel cell-culture paradigm and analyses of prion infected brain samples. Our data underscore Sho as a pre-symptomatic marker of prion infections. For PrPC alternative conformations of the N-terminal region – denoted “components 1, 2 or 3” – are known occur in the presence of different concentrations of copper (II)2. To test the hypothesis that different N-terminal PrP conformations drive different phenotypic endpoints, reiterative peptide mutagenesis was performed to produce octarepeat variants with discrete component 1 or component 3 copper-binding geometries, and DNA sequences encoding these “geometry-locked” allelic variants were then engineered to create novel lines of transgenic (Tg) cells and Tg mice. Tg mice encoding component 1 and 3 PrPC had an unusual patterns of disease susceptibility, and, most surprisingly, of endoproteolytic processing. Thus unstructured N-terminal sequences lying outside of PrPC’s three helix bundle C-terminal domain can affect physiological outcomes and are of potential relevance to both AD and prion disease pathogenesis.
Marco A.M. Prado (Robarts Research Institute & Univ. of Western Ontario, Canada)
Prion protein: a master regulator of signaling in health and disease
The prion protein is a GPI-anchored protein present in neurons whose change in conformation has been implicated in a number of neurodegenerative diseases, known as transmissible spongiform encephalopathy or prion diseases. In these diseases it is still unclear how the change in conformation of the prion protein causes neuronal death. Many potential physiological functions have been proposed for the prion protein, however there is no consensus whether any of these functions can play major roles in prion diseases or other neurodegenerative diseases. We have proposed that the prion protein can regulate neuronal signaling by scaffolding ligands and neurotransmitter receptors at the cell surface and therefore regulating neuronal function and survival. Distinct proteins have been indentified that activate neuronal signaling in a prion protein-dependent way. This leads to activation of distinct neurotransmitter receptors providing increased flexibility to neuronal signaling with consequences for neuronal differentiation and survival. One of the most studied ligands for the prion protein is STI1, a conserved co-chaperone thought to link the Hsp70/Hsp90 chaperone machinery. In addition to its intracellular functions, STI1 is secreted by distinct cells and activates multiple signaling pathways via the prion protein. However, whether STI1 has unique roles in mammals is unknown. We generated STI1 knockout mice and found that STI1 is a maternal-effect gene required for early embryonic development. MEFs lacking STI1 showed increased levels of cellular stress, did not proliferate and died after few days in culture. This phenotype could be rescued in mice by transgenic expression of a Bacterial Artificial Chromosome containing the STI1 gene. In order to further determine if STI1 levels regulate response to cellular stress we used heterozygous STI1 mutant mice. Treatment of cultured neurons with Aβ oligomers, the main culprits in Alzheimer’s disease, demonstrates that STI1 heterozygous neurons are more sensitive than wild-type neurons to cell death. The effect of Aβ oligomers could be prevented by treating neurons with recombinant STI1. Moreover, recombinant STI1 also prevented the inhibitory effects of Aβ oligomers on LTP. Mechanistically, STI1 impaired the binding of Aβ oligomers to the prion protein. Our data suggest that STI1 has unique co-chaperone functions during development that cannot be replaced by other co-chaperones. Moreover, STI1 levels regulate the response of cells to stress by binding to the prion protein. These results provide a novel framework to understand how the prion protein regulates neuronal signaling with implications for neurodegenerative diseases.
Coffee break
Doug P. Munoz (Queen's Centre for Neuroscience Studies, Queen’s Univ., Canada)
Using eye movements to probe deficits in cognition and sensory motor control in normal and abnormal aging
There is an urgent need to identify key biomarkers of normal and abnormal aging to optimize healthy aging. The MUNOZ lab uses the saccadic eye movement system to probe sensory, motor and cognitive function in normal and abnormal aging. Anatomical, physiological, clinical, and imaging studies have contributed to our extensive knowledge of the neural circuit that controls saccadic eye movements (Munoz and Everling 2004; Munoz and Coe 2011), spanning specific regions of parietal and frontal cortices, basal ganglia, thalamus, superior colliculus, cerebellum, and brainstem reticular formation. Many of these areas of the brain are known to change in structure and function during normal and abnormal aging. Eye movement tasks, in which visual stimuli are presented on a computer screen and eye movements are recorded with a video-based eye tracker, can be designed to probe specific aspects of sensory, motor, and cognitive function that are known to change during aging. This can be combined with functional brain imaging to investigate the neural substrate controlling the behaviour. Detailed quantitative assessment of eye movement behaviour can reveal functional markers for abnormal aging. This talk will have two aims: 1) review the latest progress in using the eye movement system to study aging; and 2) introduce recent work devoted to the creation of an animal model of Alzheimer’s disease that can be used to probe molecular, cellular, systems, and behavioural aspects of the disease.
Fernanda G. De Felice (Inst. Medical Biochemistry, Federal Univ. of Rio de Janeiro, Brazil)
Defective brain insulin signaling in Alzheimer’s disease
Alzheimer’s disease (AD) has been linked to defective brain insulin signaling, a proposed third type of diabetes. Although this intriguing connection between AD and diabetes has been suggested, a major unknown is the mechanism underlying brain insulin resistance in AD. We found that serine phosphorylation of IRS-1 (IRS-1pSer) is a common denominator to both diseases. Alzheimer brain tissue was found to present elevated levels of IRS-1pSer and activated JNK, analogous to what occurs in peripheral tissue in diabetes. A molecular basis for this elevation was found in the ability of Aβ oligomers, synaptotoxins that accumulate in Alzheimer brain, to trigger endoplasmic reticulum (ER) stress, activate the JNK/TNF-α pathway and cause IRS-1 inhibition in mature cultured hippocampal neurons. Impaired IRS-1 signaling and ER stress was also verified in APPSwe,PS1deltaE9 transgenic mice hippocampi. Intracerebroventricular injections of Aβ oligomers triggered hippocampal IRS-1pSer and JNK activation as well as ER stress in cynomolgus monkeys. Activation of insulin signaling by insulin and GLP-1 agonists, novel anti-diabetic drugs, prevented oligomer-induced neuronal pathologies, decreasing hippocampal IRS-1pSer, activated-JNK and markers of ER stress levels and improved cognition in transgenic mice. By establishing molecular links between dysregulated insulin signaling in Alzheimer’s and diabetes, results open avenues for rapid implementation of novel and safe therapeutics in AD.
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December 6th
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Session 5: Advanced approaches to study brain/circuit structure and function in health and disease
Kerstin Schmidt (Brain Institute - Federal Univ. Rio Grande do Norte, Brazil)
Multiplicative mechanism of lateral interactions revealed by controlling interhemispheric input
Visual information is likely to be encoded in the distributed and simultaneous activity of many neurons at different cortical stages. In agreement, response modulation by visual context from outside the classical receptive field or top-down attention occurs already in early visual areas. Modulatory influences are probably mediated by lateral or feedback connections from higher visual areas (Angelucci and Bullier, 2003; Gilbert and Sigman, 2007). We aim to characterize the nature of the modulatory influence by the lateral network. By combining reversible thermal deactivation of remote interconnected areas with optical and electrical recordings in V1 we can experimentally compare neuronal responses in primary visual cortex in four different states: intact versus interrupted lateral network with or without (spontaneously driven) visual input. When interrupting the lateral network by cooling we observe stimulus-dependent differences in the ratio of excitatory and inhibitory influences and also in the influence on stimulus-driven response variability. Responses to stimuli of lower saliency as opposed to high-contrast oriented gratings benefit more from the intact network in the sense of receiving more excitatory lateral input. In general, firing rate changes can be described by a linear model revealing a dominant multiplicative and a minor additive scaling of the baseline tuning curves. We conclude that the quantitative action of long-range horizontal connections is dynamic, depending on how the network is driven by an external stimulus. Qualitatively, those connections seem to adjust the response gain of neurons, thereby preserving their selectivity.
Timothy H. Murphy (Graduate Program in Neuroscience, Univ. British Columbia, Canada)
Imaging and Optogenetic Tools for Elucidating Cortical Circuit Function Following Stroke
During stroke, neurons can show signs of structural damage after as little as 2 min of ischemia. Over time, surviving brain tissue is thought to compensate for regions lost to stroke. It is assumed that recovery is a process that occurs over weeks and involves both the formation of new structural circuits and the alternative use of spared circuits. In mouse we show that targeted ischemia to even a single arteriole causes alterations in the patterns of sensory-evoked activity that extend beyond peri-infarct areas into somatotopic regions of the unaffected hemisphere as early as 30 min after stroke onset. These findings suggest that existing sensory pathways are capable of rapidly redistributing activity. To assess changes in functional connectivity after stroke, we have developed an automated approach to monitor intrahemispheric and interhemispheric functional relationships by the activation of ChR2-expressing cortical neurons at arbitrary cortical points in transgenic mice. To monitor regional cortical activity we employ organic voltage sensitive dyes. We extend the point stimulation to areas targeting association cortices and secondary somatosensory regions that are inaccessible to direct stimulation via the senses and could potentially contribute to reorganized circuitry. We apply graph theory and complex network analysis to connection matrices derived from these functional maps to elucidate reciprocal connections between primary and secondary sensory areas, identify network hubs, and determine asymmetries in intracortical connectivity. We anticipate that new optogenetic approaches to both monitor and manipulate neuronal function are important to describe how spared cortical circuits compensate for brain tissue lost to stroke.
Coffee break
Dora Angelaki (Dept. Neuroscience, Baylor College of Medicine, USA)
Merging of our senses: Building blocks and canonical computations
A fundamental aspect of our sensory experience is that information from different modalities is often seamlessly integrated into a unified percept. Recent computational and behavioral studies have shown that humans combine sensory cues according to a statically optimal scheme derived from Bayesian probability theory; they perform better when two sensory cues are combined. We have explored multisensory cue integration for self-motion (heading) perception using both visual (optic flow) and vestibular (linear acceleration) signals. A neural correlate of this interaction during a heading direction discrimination task is found in the activity of single neurons in the macaque visual cortex. Neurons with congruent heading preferences for visual and vestibular stimuli show improved sensitivity and lower neuronal thresholds under cue combination. In contrast, neurons with opposite preferences show diminished sensitivity under cue combination. Congruent neurons also show trial-by-trial re-weighting of visual and vestibular cues, as expected from optimal integration, and population responses can predict the main properties of perception. The trial-by-trial re-weighting can be easily simulated using a divisive normalization model extended to multisensory integration. Whereas congruent multisensory cells increase self-motion precision, oppositely-tuned multisensory cells are specialized for solving a fundamental ambiguity of the visual system, that of distinguishing motion of the objects around us versus our own motion through space. Deficits in behavior brought by chemical inactivation provide further support of the hypothesis that extrastriate visual cortex mediates multisensory integration for motion perception. These findings provide the first behavioral demonstration of statistically-optimal cue integration in non-human primates and identify both the computations and neuronal populations that may form its neural basis. Diseases, like autism spectrum disorders, might suffer from deficits in one or more of these canonical computations, which are fundamental in helping merge our senses to interpret and interact with the world.
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Final remarks and farewell
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The 2nd International Symposium “Frontiers in Neuroscience” will gather researchers working in strategic areas that represent the many facets of modern neuroscience. The program covers areas ranging from evolution of the nervous system to recent advances in neurotechnologies.
