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The mammalian neocortex is our most complex organ and plays an indispensable role in many human behaviors. Impaired function of cortical circuits is central to a diverse set of neurological and psychiatric diseases including autism spectrum disorders, epilepsy, schizophrenia and Alzheimer’s disease. Despite their functional and clinical importance, the cell types that comprise the neocortex and the molecular mechanisms that specify their properties and connectivity are only partly understood. The Nelson lab studies the development and function of the neocortex in the laboratory mouse using a combination of genetic, genomic and electrophysiological approaches. Question that they focus on include: “What genetic and epigenetic mechanisms allow different cell types to develop different patterns of connectivity?” “How does activity regulate the cell tyoe-specific expression of neuronal ion channels and synaptic molecules” and “How do genetic lesions that produce disease in mice and humans alter cellular physiology and gene expression?” To answer these questions they use new driver strains to genetically or virally deliver mutant alleles to specific neuronal cell types. They monitor effects on physiology and connectivity using patch clamp recording and high resolution anatomy. To evaluate changes in gene expression they have developed methods for manually sorting fluorescent neurons and performing genome-wide expression profiling. Using these approaches they have discovered some of the ion channels that mediate specific firing properties of cortical neurons and have identified physiological and molecular mechanisms that cause cortical impairment in the autism spectrum disorder Rett Syndrome. Current projects are focused on the role of cell adhesion molecules in regulating connectivity, the importance of DNA methylation for maintaining neuronal cell identity, and the molecular mechanisms of circuit homeostasis.
Physiological genomics of cortical circuits / Sacha Nelson.
Series:
Physiological genomics of neocortical circuits
Author:
Nelson, Sacha. National Institutes of Health (U.S.),
Publisher:
Other Title(s):
Physiological genomics of neocortical circuits
Abstract:
(CIT): The mammalian neocortex is our most complex organ and plays an indispensable role in many human behaviors. Impaired function of cortical circuits is central to a diverse set of neurological and psychiatric diseases including autism spectrum disorders, epilepsy, schizophrenia and Alzheimer"s disease. Despite their functional and clinical importance, the cell types that comprise the neocortex and the molecular mechanisms that specify their properties and connectivity are only partly understood. The Nelson lab studies the development and function of the neocortex in the laboratory mouse using a combination of genetic, genomic and electrophysiological approaches. Question that they focus on include: "What genetic and epigenetic mechanisms allow different cell types to develop different patterns of connectivity?" "How does activity regulate the cell tyoe-specific expression of neuronal ion channels and synaptic molecules" and "How do genetic lesions that produce disease in mice and humans alter cellular physiology and gene expression?" To answer these questions they use new driver strains to genetically or virally deliver mutant alleles to specific neuronal cell types. They monitor effects on physiology and connectivity using patch clamp recording and high resolution anatomy. To evaluate changes in gene expression they have developed methods for manually sorting fluorescent neurons and performing genome-wide expression profiling. Using these approaches they have discovered some of the ion channels that mediate specific firing properties of cortical neurons and have identified physiological and molecular mechanisms that cause cortical impairment in the autism spectrum disorder Rett Syndrome. Current projects are focused on the role of cell adhesion molecules in regulating connectivity, the importance of DNA methylation for maintaining neuronal cell identity, and the molecular mechanisms of circuit homeostasis.
