Research Associate, Stanford University, 2005-2007
Postdoctoral Fellow, University of California, Davis, 2001-2005
Postdoctoral Fellow, University of California, San Diego, 2000-2001
Ph.D., Rockefeller University, 2000
B.A., Integrated Science and B.A., Biological Sciences, 1994
|The neural circuits that govern perception and behavior are composed of networks of neurons that communicate with one another via synapses. As our brains develop, the roughly 10-20 billion neurons that comprise the human cerebral cortex are presented with the enormous and complex task of forming trillions of synapses with appropriate partners. Defects in synaptic connectivity and neural circuit development have been linked to diseases as diverse as anxiety disorders, depression, epilepsy, amblyopia, schizophrenia, intellectual disability and autism.|
The overall goal of my lab's research is to understand (1) mechanisms of formation of neural circuits that are essential for perception and behavior, and (2) how perturbations in neuronal development, especially those related to neurodevelopmental and psychiatric disorders, affect the composition and function of neural circuits.
Our primary approach is to use fluorescence imaging, often in living neurons, to study development of synapses and neurons in real-time. Time-lapse imaging is powerful since it allows us to simultaneously study spatial and temporal aspects of development. We complement our imaging with molecular genetics and pharmacological tools, in order to manipulate the expression and function of individual proteins and neuronal activity during development.
1. Understanding the cell-autonomous roles of neurotransmitter signaling in regulation of presynaptic development. Our previous work showed that presynaptic terminal development is facilitated by activation of NMDA receptors, and we now have evidence suggesting that this regulation is mediated by presynaptic NMDA receptors. We are interested in understanding more generally how presynaptic autoreceptors regulate presynaptic development and whether this regulation occurs at the level of individual synapses.
2. Understanding how
de novo autism-associated mutations affect neuronal development and contribute pathogenesis of simplex autism spectrum disorders. The biological causes of simplex ASD, with only one afflicted child per family, remain poorly understood. Recent genetic analyses have identified mutations that are unique to individuals with ASD, but whether and how these mutations lead to abnormal development is not yet known. Therefore, we are reproducing these mutations in rodent neurons and evaluating their effects on neuronal development.
3. We are also working to identify signals that promote synapse formation in the hope that they will provide novel therapeutic targets for treatment of diseases that are characterized by synaptic loss, such as Alzheimer's Disease and depression.