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Abundance of recently obtained datasets on brain structure (connectomics) and function (neuronal population activity) calls for a normative theory of neural computation. In the conventional, so-called, reconstruction approach to neural computation, population activity is thought to represent the stimulus. Instead, we propose that the similarity of population activity matches the similarity of the stimuli under certain constraints. From this similarity matching principle, we derive online algorithms that can account for both structural and functional observations.

Bio: Dmitri "Mitya" Chklovskii is Group Leader for Neuroscience at the Simons Foundation's new Flatiron Institute in New York City. He received a PhD in Theoretical Physics from MIT and was a Junior Fellow at the Harvard Society of Fellows. He switched from physics to neuroscience at the Salk Institute and founded the first theoretical neuroscience group at Cold Spring Harbor Laboratory in 1999, where he was an Assistant and then Associate Professor. From 2007 to 2014 he was a Group Leader at Janelia Farm where he led a team that assembled the largest-ever connectome. His group develops software for experimental data analysis and constructs normative theories of neural computation.

Quantum thermodynamics deals with thermodynamic effects and thermodynamic constraints (e.g. the 2nd law) that emerge in out-of-equilibrium microscopic open quantum systems, and in microscopic heat machines. Presently, the technology developed for quantum computing is sufficient for exploring quantum thermodynamic experimentally (new experimental results will be shown). On top of the second law, thermodynamic resource theory predicts additional mathematical constraints on thermal transformation of microscopic systems. Unlike the second law, these constraints cannot be related to thermodynamic observables. Consequently, they are useful for some theoretical purposes, but not for making concrete predictions on realistic scenarios. In this talk I will present a new formalism that yields additional “seconds laws” that follow the logic and structure of the standard 2nd law. While the 2nd law deals with the first moment of the energy (average heat, average work), the observables in the new laws are higher moments of the energy. I will show several scenarios where these laws provide concrete answers to “blind spots” that are not addressed by the standard 2nd law. In other cases tighter bounds are obtained compared to the standard 2nd law. Potentially, this formalism can significantly extend the thermodynamic framework, and put additional practical bounds on thermal transformations and microscopic heat machines. Finally, I will discuss the connection to quantum coherence measures and list several research directions.

Williams syndrome (WS) is a neurodevelopmental disorder caused by a heterozygous microdeletion of about 26 genes from chromosomal region 7q11.23, characterized by hypersociability and unique neurocognitive abnormalities. Of those deleted, general transcription factor II-i (Gtf2i), has been shown to affect hypersociability in WS, although the cell type and neural circuitry critical for the hypersociability are poorly understood. To dissect neural circuitry related to hypersociability in WS and to characterize the neuron-autonomous role of Gtf2i we conditionally knockedout Gtf2i in forebrain excitatory neurons and found this recapitulate WS features, including increased sociability and anxiety and neuroanatomical defects. Unexpectedly, we found that in the mutant mouse cortex 70% of the significantly downregulated genes were involved in myelination, together with a reduction in mature oligodendrocyte cells number, disrupted myelin ultrastructure and fine motor deficits. Analyzing the transcriptome in human frontal cortex, we found similar downregulation of myelination-related genes, suggesting a novel pathophysiological mechanism in WS, based on neuron-oligodendrocytes signaling deficits. Overall, our data detail the cellular processes that may lead to the WS typical phenotype and developmental abnormalities, and suggest new paths to explore and treat WS, as well as social and cognitive abnormalities.

TBA

Coral Landscapes at the Microscale
Orr Shapiro
Reef building corals rely on a tightly regulated symbiosis between the coral animal, endocellular microalgae, and additional microbial components. The complex network of chemical and metabolic interactions is collectively known as a holobiont. Coral pathogens disrupt these interactions, leading to the breakdown of the symbiosis and death of the coral host. Over the past decades, under warming climate and increased anthropogenic pressure, coral disease outbreaks are becoming both more frequent and more widespread, raising concerns regarding the future of these important ecosystems. Elucidating the microscale processes underlying coral disease is inherently difficult due to the physical and biochemical complexity of the different microenvironments formed around and within the coral colony. In my talk I will present a number of microfluidic-based systems developed specifically to study corals, and coral-pathogen interactions, at the microscale, and the multiple new insights we have thus far gained from bringing this type of live-imaging approach into the study of reef building corals.