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Eric S. Tucker, PhD

Associate Professor

Eric Tucker

304-293-0590

Affiliations

Physiology, Pharmacology, & Neuroscience; Blanchette Rockefeller Neurosciences Institute

Graduate Training

Cell Biology and Anatomy/Neuroscience, University of Arizona

Fellowship

Developmental Neurobiology, University of North Carolina at Chapel Hill 

Research Interests

My laboratory takes cellular, molecular and genetic approaches to study mammalian forebrain development. In particular, we focus our attention on GABAergic interneurons of the cerebral cortex, which are key cellular targets in the pathogenesis of multiple neurodevelopmental disorders including schizophrenia and autism. Our goal is to identify molecular mechanisms that underlie the generation, migration, and differentiation of cortical interneurons, and provide insight into how disruptions in cortical development may result in neurological and psychiatric illnesses. 

Techniques Include:

Mouse genetics/embryology
Electroporation 
Organotypic tissue culture
Primary neuronal cell culture
Immunocytochemistry 
Molecular biology 
Biochemistry
Confocal microscopy
Live-cell imaging

Research Topics

Development of cortical interneurons

Most cortical interneurons are generated from progenitor cells located in the medial and caudal ganglionic eminences (MGE and CGE), which are anatomically defined and molecularly distinct compartments of the developing ventral forebrain. MGE progenitors produce parvalbumin- and somatostatin-positive cortical interneurons, while CGE progenitors produce cortical interneurons that label for calretinin and VIP. In contrast, progenitors in the neighboring lateral ganglionic eminence (LGE) produce interneurons destined for the granule and periglomerular layers of the olfactory bulb. The molecular mechanisms that underlie the differential production of cortical interneurons in the MGE and CGE, and the selective generation of olfactory bulb interneurons in the LGE, are presently unknown. As a postdoctoral fellow, I found that migratory specificity of MGE and LGE cells is acquired from their progenitors, irrespective of their placement in the ventral forebrain. Subsequently, I uncovered novel molecular distinctions that further delineate LGE, MGE, and CGE progenitors, and identified the frontonasal mesenchyme as a potent modulator of ventral forebrain patterning. My lab is now exploring how cellular diversity amongst ventral forebrain progenitors is functionally translated into the unique migratory and differentiation programs of their post-mitotic progeny. Currently, we are asking how newly identified MGE genes participate in the genesis, migration, and differentiation of MGE-derived cortical interneurons. One MGE-enriched gene, Map3K12 binding inhibitory protein 1 (Mbip), was originally identified as a negative regulator of c-Jun kinase (JNK) signal transduction, but its function in brain development has not yet been determined. In initial experiments we find that Mbip regulates neuronal migration, and accordingly, we are examining how Mbip, and more broadly, JNK signaling, contributes to cortical interneuron development. 

Lab Personnel

Abigail Myers 
Neuroscience Graduate Student
akmyers@mix.wvu.edu

Skye Hickling
Neuroscience Graduate Student
sehickling@mix.wvu.edu

Catherine Smith
Neuroscience Graduate Student
ctsmith2@mix.wvu.edu

Steven Shaffer
Laboratory Technician
steven.shaffer@hsc.wvu.edu

Several graduate student positions are available. If interested, please contact me to arrange a rotation!

Publications

[2015]

[2014]

[2012]

[2011]

[2010]

[2009]

[2008]

[2006]