Barbara Thompson, PhD

Assistant Professor of Occupational Science and Occupational Therapy

Room: CHP 133
Phone: (323) 442-2850
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Biography

Barbara Thompson was most recently Research Assistant Professor at the Keck School of Medicine of USC, Department of Cell and Neurobiology. She had previously been a Postdoctoral Fellow at Vanderbilt University Medical Center's Department of Pharmacology. Dr. Thompson has conducted groundbreaking research in the neurobiology of developmental disorders and is contributing to the development of translational science in areas such as autism by developing and testing conceptual models which link clinical problems in human populations to animal studies in the neurosciences. Dr. Thompson has already demonstrated particular skill in interdisciplinary research collaborations and strengthens the Division’s critical mass in autism and sensory integration with a special focus on neuroscience research.

Education

Doctor of Philosophy (Ph D) in Psychology
Univ Delaware
2003

Bachelor of Science (BS) in Psychology
Florida State University
1997

Publications

Journal Articles

Eagleson, K. L., Campbell, D. B., Thompson, B. L., Bergman, M. Y., & Levitt, P. R. (2011). The autism risk genes MET and PLAUR differentially impact cortical development. Autism Research, 4(1), 68-83. Abstract →← Abstract 

Candidate risk genes for autism spectrum disorder (ASD) have been identified, but the challenge of determining their contribution to pathogenesis remains. We previously identified two ASD risk genes encoding the receptor tyrosine kinase MET and the urokinase plasminogen activator receptor (PLAUR), which is thought to modulate availability of the MET ligand. We also reported a role for Met signaling in cortical interneuron development in vitro and a reduction of these neurons in uPAR (mouse ortholog of PLAUR) null mice, suggesting that disruption of either gene impacts cortical development similarly. Here, we modify this conclusion, reporting that interneuron numbers are unchanged in the neocortex of Met(fx/fx) / Dlx5/6(cre) mice, in which Met is ablated from cells arising from the ventral telencephalon (VTel). Consistent with this, Met transcript is not detected in the VTel during interneuron genesis and migration; furthermore, during the postnatal period of interneuron maturation, Met is co-expressed in glutamatergic projection neurons, but not interneurons. Low levels of Met protein are expressed in the VTel at E12.5 and E14.5, likely reflecting the arrival of Met containing corticofugal axons. Met expression, however, is induced in E12.5 VTel cells after 2 days in vitro, perhaps underlying discrepancies between observations in vitro and in Met(fx/fx) / Dlx5/6(cre) mice. We suggest that, in vivo, Met impacts the development of cortical projection neurons, whereas uPAR influences interneuron maturation. An altered balance between excitation and inhibition has been postulated as a biological mechanism for ASD; this imbalance could arise from different risk genes differentially affecting either or both elements.

Thompson, B. L., & Levitt, P. R. (2010). The clinical-basic interface in defining pathogenesis in disorders of neurodevelopmental origin. Neuron, 67(5), 702-712. Abstract →← Abstract 

Human cognitive and social-emotional behaviors are heterogeneous, underscoring the challenges in modeling pathogenesis in disorders of neurodevelopmental origin in which these domains are dysfunctional. In general, animal models for these disorders are built to emulate our understanding of the clinical diagnosis, with mixed results. We suggest the utility of model systems lies in the use of different strategies to perturb hierarchical circuit development, to examine the behavioral dimensions that are most impacted, and to discern the capacity for, and heterogeneity of, neuroadaptation that will then inform treatment strategies.

Thompson, B. L., & Levitt, P. R. (2010). Now you see it, now you don’t—Closing in on allostasis and developmental basis of psychiatric disorders. Neuron, 65(4), 437-439. Abstract →← Abstract 

The mode through which early insults in brain development result in the onset of psychiatric disorders years after impact become a little less mysterious with the report by Niwa et al. that a transient reduction of the schizophrenia risk gene DISC1 can alter prefrontal cortex neurochemistry, architecture, and function.

Thompson, B. L., Stanwood, G. D., & Levitt, P. R. (2010). Specificity of prenatal cocaine exposure effects on cortical interneurons is independent from dopamine D1 receptor co-localization. Journal of Chemical Neuroanatomy, 39, 228-234. Abstract →← Abstract 

Gestational cocaine exposure in a rabbit model leads to a persistent increase in parvalbumin immunoreactive cells and processes, reduces dopamine D1 receptor coupling to Gsalpha by means of improper trafficking of the receptor, changes pyramidal neuron morphology, and disrupts cognitive function. Here, experiments investigated whether changes in parvalbumin neurons were specific, or extended to other subpopulations of interneurons. Additionally, we examined dopamine D1 receptor expression patterns and its overlap with specific interneuron populations in the rabbit prefrontal cortex as a possible correlate for alterations in interneuron development following prenatal cocaine exposure. Analysis of calbindin and calretinin interneuron subtypes revealed that they did not exhibit any differences in cell number or process development. Thus, specific consequences of prenatal cocaine in the rabbit appear to be limited to parvalbumin-positive interneurons. Dopamine D1 receptor expression did not correlate with the selective effects of cocaine exposure, however, as both parvalbumin and calbindin cell types expressed the receptor. The findings suggest that additional, unique properties of parvalbumin neurons contribute to their developmental sensitivity to in utero cocaine exposure.