Stanford Neurosciences Institute Seminar Series Presents
Making up your mind, the specification and integration of interneurons into cortical networks
Gordon Fishell, Ph.D
Julius Raynes Professor of Neuroscience and Physiology, Department of Neuroscience and PhysiologyProfessor, Department of Neurology, Associate Director of Neuroscience Institut, New York University (NYU)
Host: Kristin Muench (Palmer Lab)
My talk will be focused on two complementary aspects of cortical interneuron development. Firstly, from a developmental genetics vantage we are examining the trajectories by which cortical interneurons are generated from their anlage, the three ganglionic eminences, the medial, lateral and caudal ganglionic eminences. Historically, this has involved fate mapping these progenitor zones (Wichterle et al., 2001; Nery et al., 2003, Butt et al., 2005, Miyoshi et al., 2007, 2010). More recently this work has been complemented by single cell RNA-seq analysis (Mayer et al., in preparation) demonstrating the underlying logic by which interneuron and projection neurons are specified during development.
Secondly, the laboratory has increasing intrigued by postnatal events by which cortical interneurons become integrated into brain circuits. Beginning with the recognition that modulation of activity can affect both the migration and morphological development of interneurons (De Marco et al., 2011), the laboratory has become interested in the connection between activity and gene expression (Demarco et al., 2015). In an effort to determine the endogenous sources of activities critical to the assembly of the microcircuits that interneurons contribute to we have also used a combination of monosynaptic rabies tracing and optogenetics to query the connectivity of interneurons within developing cortex (Tuncdemir et al., 2016). An theme emerging from these studies is that the developmental and genetic events required for cortical interneurons to properly develop when perturbed may be a proximal cause for some forms of neuropsychiatric disease (Karayannis et al., 2014).