Author: Julie Pryor

Brain disorders, climate change, clean energy, cancer – these are examples of problems which are difficult to solve because we don’t know what we would need to know to solve them. Edward Boyden, Associate Professor at Massachusetts Institute of Technology, teaches students how to think about approaching intractable problems. In this presentation for the World Economic Forum, he explains strategies such as valuing interdisciplinary expertise and being willing to leave comfort zones.

Title: “Neural computations in the retina: from photons to behavior”
Speaker: Markus Meister, Caltech
Date + Time: March 8, 2016 @ 4pm
Location: 46-3002 (Singleton Auditorium)

Abstract:

The retina is touted as the brain’s window upon the world, but unlike a glass pane, the retina performs a great deal of visual processing. Its intricate circuits use ~70 different types of neuron. The output signals in the optic nerve are carried by 20 different types of retinal ganglion cell, each of which completely tiles the visual field. Thus the eye communicates twenty parallel representations of the visual scene. This raises several questions: What is being computed here, can we understand the visual feature reported by each type of ganglion cell? How is this feature computed by the circuit of neurons and synapses that leads to that ganglion cell type? And finally, why are these particular features getting computed, rather than some other set? In recent years, all these research areas have been turbocharged by modern genetic tools, especially the ability to visualize and modify select neuron types within a circuit. Some general insights are:

What? The various ganglion cell types fit on a spectrum from simple “pixel encoders” to “feature detectors”. A few types encode a very simple function of the image, like the local contrast, with a continuously varying firing rate. However, most types fire quite rarely and report specific features, for example differential motion between the foreground and the background. Some ganglion cells seem to play an alarm function; they are silent except under very specific stimulus conditions associated with threats.

How? It has emerged that dramatically different computations can result from circuits using the same kinds of neuronal elements, but arranged in a different sequence or combinations. In fact many of the twenty circuits in the retina share the same elements. On at least one occasion the same neuron is used to transfer signals in both directions! An important source of nonlinearity on which the computations are based is the sharp thresholding of signals at the bipolar cell synapse, which has emerged as a very versatile circuit element.

Why? It has been proposed that each of the twenty ganglion cell types of the retina is Evolution’s answer to a specific behavioral need that is served by the visual system. If so, then the selective silencing of one type of ganglion cell should affect only selected visual behaviors. Early experiments suggest this is a promising avenue of research.

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.