Author: Julie Pryor

In the Chinese calendar, 2016 is the Year of the Monkey. We wish all of our friends and colleagues a happy, healthy and inventive new year!

“Connectomics and Psychopathology: A Tale of Many Regions”

Abstract: A growing body of research clearly indicates that both functional and structural connectivity within and between core brain systems is a critical determinant of cognitive and affective function in both health and disease. This talk will first briefly overview the state of the art methods for assessing human brain connectivity. Next this talk will illustrate the ways in which variation in brain connectivity relates to variation in cognitive and affective functions in healthy individuals, as well as how impairments in functional brain connectivity relate to impaired cognitive and affective function associated with risk for psychopathology and manifest illness.

Gordon Fishell, PhD
Julius Raynes Professor of Neuroscience, Associate Director of the NYU Neuroscience Institute

My laboratory is interested in the developmental steps that allow the startling repertoire of interneurons to develop and integrate into the developing nervous system. This process begins with their specification during which genetic programs initiated within progenitors relegate interneurons into specific cardinal classes. Subsequent to this neuronal activity is fundamental for both the laminar positioning, as well as the dendritic and axonal arborization of at least some interneuron subtypes. These results suggest that sensory information complements earlier established genetic programs to shape the way interneuronal subtypes integrate into nascent cortical circuits. The challenge moving forward is to understand how genetically similar interneuron subtypes are able to incorporate into diverse circuitries as different as the inhibitory circuitry that makes up the basal ganglia versus the excitatory circuits that make up the cerebral cortex.

Scientists have long wondered if the human brain contains neural mechanisms specific to music perception. Now, for the first time, MIT neuroscientists have identified a neural population in the human auditory cortex that responds selectively to sounds that people typically categorize as music, but not to speech or other environmental sounds.

Recent advances in high throughput genomic technologies, coupled with large patient cohorts and and an evolving culture of rapid data sharing have led to remarkable advances in the understanding of the genetics of autism spectrum disorders. To date, the lion’s share of this progress has been with regard to the contribution of rare and de novo mutations, both in DNA sequence and chromosomal structure. The ability now to reliably and systematically identify ASD risk genes and loci provides important initial insights into both the opportunities as well as the challenges the field now faces in moving from gene discovery to an actionable understanding of pathophysiological mechanisms underlying these complex common neurodevelopmental syndromes. The lecture will provide an overview of what is now known about the genomic architecture and specific risk mutations associated with ASD, address the particular challenges posed by the discovery of mutations that have large biological effect but low population allele frequency, and consider the role that whole genome sequencing will play in the near future in enhancing the understanding of the developmental aspects of ASD risk.

Stanley Center & Poitras Center Translational Neuroscience Joint Seminar
Speaker: Amy Arnsten, Yale University
December 1, 2015

The newly evolved circuits of the primate dorsolateral prefrontal cortex (dlPFC) generate the mental representations needed for working memory, the foundation of abstract thought. These layer III dlPFC pyramidal cell microcircuits are a focus of pathology in cognitive disorders such as schizophrenia and Alzheimer’s Disease. Research in the Arnsten lab has found that these circuits are uniquely regulated at the molecular level in ways that facilitate mental flexibility but make them particularly vulnerable to atrophy and degeneration. For example, in contrast to the primary visual cortex where calcium-cAMP signaling strengthens connections and increases neuronal firing, increased calcium-cAMP signaling in layer III of dlPFC weakens connections and decreases neuronal firing by opening K+ channels near the synapse. Understanding these unique properties has led to the development of treatments for dlPFC cognitive disorders in humans, e.g. Intuniv™, illustrating the importance of translational research.