BBI Special Seminar: Anthony LaMantia, Establishing cerebral cortical circuits for complex behavior

Tuesday, June 4, 2019
11:00 a.m.
0215 Edward St. John Center

Establishing cerebral cortical circuits for complex behaviors

Anthony LaMantia
Lieberman Professor of Neuroscience
Director, GW Institute for Neuroscience
Professor, Anatomy & Cell Biology
George Washington University School of Medicine & Health Services

Abstract
Neural circuits that specify essential behaviors are thought to have equally specified templates for development. Indeed, strategies and genetic architectures for sensory and motor systems differentiation have begun to be delineated. These discoveries provide critical understanding of each system’s capacities as well as insight into how dysfunction arises and deficits might be improved. In contrast, far less is known about developmental or genetic mechanisms that account for circuits underlying complex cognitive or social behaviors, especially in mammals. We defined a developmental mechanism, and its genetic basis, for association cortical connections that mediate a complex “cognitive” behavior. This behavior —a visual reversal task—relies not only on sensory processing or motor output, but on the capacity to detect a learning rule, and the flexibility to reverse that rule. We defined the developmental mechanism for the circuit that mediates this behavior in the mouse, using typically developing mice as well as those carrying a genomic lesion—deletion of orthologues of genes deleted heterozygously in the human deletion disorder, DiGeorge/22q11.2 Deletion Syndrome (22q11DS). Cellular, genetic and behavioral analysis of the 22q11DS mouse model, defines a specific strategy for association cortico-cortical circuit development that facilitates the capacity for a complex “cognitive” behavior.

Biography
Anthony LaMantia received his B.A. from the University of Chicago in 1982 and his Ph.D. from Yale University in 1988. His work explores genetic and molecular mechanisms of early forebrain development, particularly signaling and transcriptional regulation of forebrain stem cell identity and the role of forebrain developmental regulatory genes in behavioral and psychiatric diseases including schizophrenia and autism. In addition, he has an ongoing research interest in molecular mechanisms that specify neural stem cells in the embryonic as well as adult nervous system. The mechanisms that maintain this stem cell provide a superb model for considering neuronal regeneration as well as degenerative disorders including Alzheimer’s and Parkinson’s Disease that disrupt the ongoing replacement of olfactory sensory neurons.

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