My lab uses animal models to understand how neuromodulators contribute to sensory and memory encoding and how this can facilitate interactions across regions of the brain. We utilize optogenetic and chemogenetic targeting tools to measure how perturbations of neurotransmitter systems associated with illness or disease alter sensory encoding and the coupling of neurons and brain regions together to ultimately influence learning and memory or cognitive and social behavior in mice.

1. OSCILLATIONS IN CIRCUIT FUNCTION

How do distinct regions of the brain interact as a process of what we experience and how does that information modulate perception? It is a mystery as to how coordination between brain regions occurs, but overwhelming evidence suggests that rhythms or “brain waves” that are present in all animal species serve as a type of scaffolding that allow for the dynamic coupling of regions together transiently. In diseases such as autism, we believe that local rhythms contribute so strongly to couple nearby neurons that they are not influenced by other regions of the brain. In contrast, in conditions like Parkinson’s disease, we believe that regions of the motor pathways become so ubiquitously over-coupled that it impedes the ability to promote movement. We aim to understand the mechanisms important for the generation and timing of rhythms that temporally couple neurons and how this process aids cognitive performance and how changes in normal rhythms can contribute to neuropsychiatric illness and disease.

2. TOP-DOWN REGULATION OF SENSORY PROCESSING

What is the role of “top-down” or cognitive control in  sensory processing and neural plasticity? We are constantly bombarded with sensory information some of which is entirely irrelevant to what we experience or remember. Our ability to attend or filter only the most relevant stimuli in our environment is advantageous to survival although the cortical processes that underlie such behavior is not well understood. Our lab takes a neuroethological approach to understand how cortical circuits important for decision making and motivated behavior can sculpt what we hear, see, and remember. Furthermore, we are driven to understand how this processes is altered in neurodevelopmental  disorders or aging where reduced cognitive control has been implicated in disorders of sensory processing.

3. UNCERTAINTY IN DECISION MAKING

What are the neural underpinnings of uncertainty in decision making and how do attentional mechanisms modify that process? Our lab studies how previous experience contributes to expectations and the role of cognitive control in modifying behavior when our expectations are not met. To do so, we apply novel imaging or electrophysiology techniques with cognitive behavior during extinction and reversal learning tasks. Our work focuses on the prefrontal cortex (PFC) and the role of cognitive control when action-outcome expectations change.

4. HOMEOSTATIC REGULATION OF NEURAL CIRCUITS

How is information processing regulated with neural circuits and how does imbalance in neuromodulators and excitation/inhibition contribute to neuropsychiatric illness? Imbalances between excitation and inhibition (E/I) represent a common pathological feature in neurodevelopmental and neurodegenerative disorders such as Parkinson’s Disease and Autism. A variety of genetically distinct disease models commonly share imbalanced synaptic conductance ratios and abnormal brain oscillations. Despite the shared prevalence of E/I imbalance, abnormal rhythms, and the presence of motor, social, or cognitive deficits, there is no underlying unifying theory to connect these features. Our lab is interested in identifying the mechanistic foundation of imbalance and how does imbalance contribute to cognitive or behavioral deficits using high density recordings from known cell types across aging and disease.