In Situ Hybridization

In situ hybridization showing reduced expression after prenatal stress of key transcription factors for inhibitory neuron development.

Prenatal stress mechanisms and embryonic development of inhibitory neurons

Our lab has shown that prenatal stress delays inhibitory neuron migration and downregulates the expression of key transcription factors involved in inhibitory progenitor development. We are currently examining how much of these effects may be due to glucocorticoids, immune activation and other maternal factors.

Supported by a Patterson Trust Award Program in Clinical Research

Postnatal neurobiological and behavioral trajectories after prenatal stress

We are currently examining the relationship between alterations in the neurobiology of inhibitory neurons, glial cells and behavior in prenatally-stressed mice. 

Supported by a NIMH Career Development Award

Gene-environment interaction and ADHD: translation between rodent and human models of prenatal stress, genetic risk, and postnatal environment

In an extension of our work in fibroblast growth factor receptors and prenatal stress as above, we are currently collaborating with David Reiss and the Early Growth and Development Study. We are examining adopted children in order to understand the interaction of different risk factors for attention-deficit disorder.

Supported by a Klingenstein Third Generation Foundation Fellowship in Attention Deficit Hyperactivity Disorder

The role of Fibroblast Growth Factor 2 in the impact of prenatal stress

Growth factors play important roles in early developmental processes in the CNS. Interactions between genes and environment are significant in the etiology of psychiatric disorders. In collaboration with the Vaccarino lab, we are exploring the interaction between growth factor genes and prenatal stress as risk factors for behavioral changes in activity level and working memory.

Supported by a Klingenstein Third Generation Foundation Fellowship in Attention Deficit Hyperactivity Disorder & a Brain and Behavior Research Foundation Young Investigator Program award

Adult BCKDK KO female (left) and male (right) mice showing reduced fur and whiskers on snout.

BCKDK mice as a model for autism

Recent findings have implicated mutation of the branched chain ketoacid dehydrogenase kinase (BCKDK) gene in the clinical appearance of autism, seizures and intellectual disability. A model lacking this gene, BCKDK knockout mice (KO), has neurobiological deficits including seizures. The developmental time course of abnormalities in this model is unknown but some are preventable with a high protein diet. Neurodevelopmental studies in mouse models are essential for understanding the mechanisms by which abnormalities arise and determining methods for treating the pathology of autism. Little detailed neurobiological information about this model is known. The goals of this project are to examine this model of autism developmentally using molecular, electrophysiological, and behavioral approaches.
Time Lapse of Migrating Interneurons

Time Lapse of Migrating Interneurons

60 minute pilot confocal time lapse imaging of GAD67GFP+ cells in an E14 forebrain section in vitro