Current research projects
Our lab works to understand how neural synchrony shapes information processing, and how that synchrony is altered in cognitive disorders.
The brain depends on precisely timed neuronal activity to control behavior. In the hippocampus, neurons fire in-sync with theta oscillations – rhythmic brain waves occurring at about 5 to 12 times per second — creating windows of time in which neurons can work together to drive cognition. Inhibitory neurons are especially tightly locked to this rhythm, helping route information and keeping excitation and inhibition in balance. However, most of what we know about this timing comes from correlation, inferred from disease cases where it breaks down.
Our lab works to directly manipulate neural timing to uncover how disruptions in spike timing cause cognitive impairment, and how restoring proper timing can rescue function. Using closed-loop systems, we test how the synchrony of inhibitory neurons shapes plasticity and cognition, both in the healthy brain and in the context of epilepsy and aging.
Strong evidence from the aging field suggests that maintaining hippocampal neural synchrony and excitability into middle age confers resilience against cognitive decline, with the severity of hippocampal deficits correlating with cognitive impairment. Our lab explores this by directly manipulating inhibitory spike timing and determining how cell-network synchrony impacts cognitive decline during physiological aging.
Characterizing cell-network synchrony breakdowns during aging
Using optogenetic tagging strategies, coupled with cognitive batteries, we explore whether inhibitory subtypes lose their spike timing precision during the critical transition from healthy aging to cognitive decline.
Neural synchrony in information processing
We explore whether restoring inhibitory theta phase locking in middle-aged animals will improve hippocampal task performance, while disrupting timing in young adults will accelerate aging-like cognitive impairments.
Theta phase of neural activity can control network reorganization by providing a temporal window for enhanced plasticity — stimulating neuronal activity during one theta phase can facilitate long-term potentiation, while stimulation during the opposite phase induces long-term depression.
Previously, we developed a tool called PhaSER, which can directly manipulate theta phase locking in real time in awake, behaving animals. This tool uniquely enables bidirectional control of individual neuron spike timing relative to endogenous oscillations while simultaneously monitoring spiking. Our lab uses this tool to explore whether stimulations delivered at specific phases of theta may produce beneficial re-organization of the epileptic hippocampal circuit and produce long-lasting, disease-modifying effects.
As our lab continues to grow, we are hopeful to apply PhaSER in different ways — with the goal of providing hope to people with epilepsy while shedding light on the fundamental mechanisms of hippocampal network dynamics. Three directions are underway:
Freely Moving Behaviors
We're extending PhaSER for use in animals during natural, unrestrained behavior.
PhaSER and Seizures
We're testing whether phase-targeted stimulation can reshape circuit activity during epileptogenesis.
PhaSER and Cognitive Deficits
We're asking whether restoring phase locking can rescue the cognitive deficits associated with epilepsy.
Our lab is interested in identifying therapies that might be applied across health and disease to prevent the onset of pathological and physiological cognitive decline. Current open questions include:
Connectivity
We're interested in brain-wide assessments of upstream regions that may show altered connectivity to the dentate gyrus in epilepsy and during pathological and physiological aging.
Long-range inhibition
We're interested in how long-range inhibition might alter cross-regional communication in epilepsy and pathological and physiological aging.
Prefrontal cortex
We're interested in whether a breakdown in theta phase locking in the prefrontal cortex underlies the emergence of working memory deficits.
Sex differences
We're interested in whether there may be sex-specific vulnerabilities in neural synchrony.
Neurofeedback
We're interested in whether animals can be trained to spend more time in a state of high phase locking using neurofeedback techniques.
Funding and Support
Thanks to these organizations for funding our research
NIH
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Simons Foundation
Simons Collaboration on Plasticity and the Aging Brain (SCPAB) Transition to Independence Award
Knight Campus
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Featured Publications
2025
Interneuron theta phase locking controls seizure susceptibility
bioRxiv, currently under review
2025
Distinct changes to hippocampal and medial entorhinal circuits emerge across the progression of cognitive deficits in epilepsy
Cell Reports
2023
Progressive Excitability Changes in the Medial Entorhinal Cortex in the 3xTg Mouse Model of Alzheimer's Disease Patholog
Journal of Neuroscience