3D motion : encoding and perception

The visual system supports perception and inferences about events in a dynamic, three-dimensional (3D) world. While remarkable progress has been made in the study of visual information processing, the existing paradigms for examining visual perception and its relation to neural activity often fail to generalize to perception in the real world which has complex dynamics and 3D spatial structure. This thesis focuses on the case of 3D motion, developing dynamic tasks for studying visual perception and constructing a neural coding framework to relate neural activity to perception in a 3D environment. First, I introduce target-tracking as a psychophysical method and develop an analysis framework based on state space models and the Kalman filter. I demonstrate that target-tracking in conjunction with a Kalman filter analysis framework produce estimates of visual sensitivity that are comparable to those obtained with a traditional forced-choice task and a signal detection theory analysis. Next, I use the target-tracking paradigm in a series of experiments examining 3D motion perception, specifically comparing the perception of frontoparallel motion with the perception of motion-through-depth. I find that continuous tracking of motion-through-depth is selectively impaired due to the relatively small retinal projections resulting from motion-through-depth and the slower processing of binocular disparities. The thesis then turns the neural representation of 3D motion and how that underlies perception. First I introduce a theoretical framework that extends the standard neural coding approach, incorporating the environment-to-retina transformation. Neural coding typically treats the visuals stimulus as a direct proxy for the pattern of stimulation that falls on the retina. Incorporating the environment-to-retina transformation results in a neural representation fundamentally shaped by the projective geometry of the world onto the retina. This model explains substantial anomalies in existing neurophysiological recordings in primate visual cortical neurons during presentations of 3D motion and in psychophysical studies of human perception. In a series of psychophysical experiments, I systematically examine the predictions of the model for human perception by observing how perceptual performance changes as a function of viewing distance and eccentricity. Performance in these experiments suggests a reliance on a neural representation similar to the one described by the model. Taken together, the experimental and theoretical findings reported here advance the understanding of the neural representation and perception of the dynamic 3D world, and adds to the behavioral tools available to vision scientists.Neuroscienc

Neuromatch Academy: Teaching Computational Neuroscience with global accessibility

Neuromatch Academy designed and ran a fully online 3-week Computational Neuroscience summer school for 1757 students with 191 teaching assistants working in virtual inverted (or flipped) classrooms and on small group projects. Fourteen languages, active community management, and low cost allowed for an unprecedented level of inclusivity and universal accessibility.Comment: 10 pages, 3 figures. Equal contribution by the executive committee members of Neuromatch Academy: Tara van Viegen, Athena Akrami, Kate Bonnen, Eric DeWitt, Alexandre Hyafil, Helena Ledmyr, Grace W. Lindsay, Patrick Mineault, John D. Murray, Xaq Pitkow, Aina Puce, Madineh Sedigh-Sarvestani, Carsen Stringer. and equal contribution by the board of directors of Neuromatch Academy: Gunnar Blohm, Konrad Kording, Paul Schrater, Brad Wyble, Sean Escola, Megan A. K. Peter

Pathogenic variants in HTRA2 cause an early-onset mitochondrial syndrome associated with 3-methylglutaconic aciduria

Mitochondrial diseases collectively represent one of the most heterogeneous group of metabolic disorders. Symptoms can manifest at any age, presenting with isolated or multiple-organ involvement. Advances in next-generation sequencing strategies have greatly enhanced the diagnosis of patients with mitochondrial disease, particularly where a mitochondrial aetiology is strongly suspected yet OXPHOS activities in biopsied tissue samples appear normal. We used whole exome sequencing (WES) to identify the molecular basis of an early-onset mitochondrial syndrome—pathogenic biallelic variants in the HTRA2 gene, encoding a mitochondria-localised serine protease—in five subjects from two unrelated families characterised by seizures, neutropenia, hypotonia and cardio-respiratory problems. A unifying feature in all affected children was 3-methylglutaconic aciduria (3-MGA-uria), a common biochemical marker observed in some patients with mitochondrial dysfunction. Although functional studies of HTRA2 subjects’ fibroblasts and skeletal muscle homogenates showed severely decreased levels of mutant HTRA2 protein, the structural subunits and complexes of the mitochondrial respiratory chain appeared normal. We did detect a profound defect in OPA1 processing in HTRA2-deficient fibroblasts, suggesting a role for HTRA2 in the regulation of mitochondrial dynamics and OPA1 proteolysis. In addition, investigated subject fibroblasts were more susceptible to apoptotic insults. Our data support recent studies that described important functions for HTRA2 in programmed cell death and confirm that patients with genetically-unresolved 3-MGA-uria should be screened by WES with pathogenic variants in the HTRA2 gene prioritised for further analysis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10545-016-9977-2) contains supplementary material, which is available to authorized users

From Puzzle to Progress: How Engaging With Neurodiversity Can Improve Cognitive Science

In cognitive science, there is a tacit norm that phenomena such as cultural variation or synaesthesia are worthy examples of cognitive diversity that contribute to a better understanding of cognition, but that other forms of cognitive diversity (e.g., autism, attention deficit hyperactivity disorder/ADHD, and dyslexia) are primarily interesting only as examples of deficit, dysfunction, or impairment. This status quo is dehumanizing and holds back much-needed research. In contrast, the neurodiversity paradigm argues that such experiences are not necessarily deficits but rather are natural reflections of biodiversity. Here, we propose that neurodiversity is an important topic for future research in cognitive science. We discuss why cognitive science has thus far failed to engage with neurodiversity, why this gap presents both ethical and scientific challenges for the field, and, crucially, why cognitive science will produce better theories of human cognition if the field engages with neurodiversity in the same way that it values other forms of cognitive diversity. Doing so will not only empower marginalized researchers but will also present an opportunity for cognitive science to benefit from the unique contributions of neurodivergent researchers and communities