Our lab is interested in the neural basis of goal-directed behavior, focusing on the roles of the prefrontal and cingulate cortices. We use the mouse as a model, and specialize in a variety of optical techniques, including two-photon calcium imaging and optogenetics, for recording and controlling neural activity in behaving mice. Through experiments at the cellular and systems levels, our long-term goal is to understand how neurons in the prefrontal cortex process information and why circuit-level dysfunctions could lead to cognitive deficits associated with neuropsychiatric disorders. Currently we are pursuing several research directions:

GABAergic Interneurons

Top-down Selective Attention

There are multiple subtypes of inhibitory interneurons in the neocortex. These cell types have distinct morphological and electrophysiological properties, suggesting specialized computational functions. Our recent results demonstrated that cortical interneurons have cell type-specific functional connectivity in vivo. Moreover, selective optogenetic activation of cortical interneuron subtypes led to distinct effects on sensory processing in behaving mice. The lab is following up on this work by investigating the role of major interneuron subtypes in the mouse prefrontal cortex for cognitive behaviors.

Adaptive Behavior and Learning

The prefrontal cortex is important for learning, especially in associating events and actions that are separated by a temporal gap. The brain region also plays a major role in "learning to learn", the ability to generate and implement behavioral strategies in a changing environment. To examine these types of adaptive behaviors, we are leveraging our experience with head-fixed mice to design new behavioral tasks. Current projects use optical imaging, optogenetics, and molecular tools to explore the neural ensemble dynamics in behaving mice.

Mouse Models of Neuropsychiatric Disorders

Mouse models of psychiatric disorders

Frontal lobe dysfunction is linked to numerous disorders including depression, schizophrenia, and Alzheimer's disease. Despite the devastating effects of these mental illnesses, we lack a reliable suite of biomarkers and a mechanistic understanding of the cognitive deficits. This is not surprising considering the complexity in both the etiology and the underlying neural circuitry, making any study that correlates these two aspects of a disorder difficult to interpret. We are working on developing chronic imaging solutions that overcome this problem by monitoring the structure and function of neuronal ensembles over time as the disorder progresses.


We are grateful for support from the NIH, Brain & Behavior Research Foundation, Inscopix, and Epilepsy Foundation.