Research
How neuronal assemblies build memory—and change in depression
Vision
The Robinson Lab investigates how neuronal assemblies—coordinated groups of neurons that fire together—form, stabilize, and communicate across hippocampal-prefrontal circuits. We combine molecular, cellular, and systems neuroscience to understand how these ensembles support memory consolidation and how their disruption may contribute to depression-like behavior.
Our goal is to bridge scales of analysis: from synapses and intrinsic cellular properties, to gene-expression programs, local microcircuits, and coordinated activity across brain regions. By identifying the mechanisms that recruit particular neurons into assemblies, we aim to reveal how experiences become stable memories and to uncover potential routes for restoring disrupted circuit function.
We will first establish mechanisms of assembly formation and stabilization in the hippocampus, then extend this framework to the prefrontal cortex. Comparing the two regions will help define how local inhibition, long-range inputs, synaptic plasticity, and transcriptional state support memory—and how these mechanisms are altered by chronic stress.
Research-program figure forthcoming.
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Research Topics
Our research program is organized around three connected questions, spanning memory, assembly membership, and circuit dysfunction.
1. Neuronal assemblies and memory consolidation
We study how hippocampal and prefrontal assemblies encode, reactivate, and consolidate spatial and episodic memories. During sleep, hippocampal sharp-wave ripples coordinate the reactivation of recent experience; prefrontal assemblies integrate these signals with task rules and contextual information. Our recent work shows that a specific subset of sharp-wave ripples drives prefrontal reactivation and that enhancing these events can improve spatial memory.
2. The synaptic and cellular basis of assembly membership
Why are some neurons recruited into an assembly while others are not? We will compare behaviorally tagged and untagged pyramidal neurons to determine how synaptic inputs, intrinsic excitability, inhibitory microcircuits, and activity-dependent molecular programs shape assembly recruitment and stabilization.
3. Hippocampal-prefrontal circuit dysfunction in depression
Using chronic social defeat stress in mice, we will test whether disrupted hippocampal-prefrontal assembly dynamics contribute to depression-like behavior. We will identify associated synaptic, cellular, and transcriptional changes, then test whether restoring ensemble activity or targeted signaling pathways can rescue circuit dynamics and behavior.
Techniques
Our work integrates activity-dependent neuronal tagging, high-density silicon-probe recordings, optotagging and closed-loop optogenetics, whole-cell patch-clamp physiology, local and long-range circuit tracing, and single-cell profiling. This toolkit lets us follow the same problem from circuit activity to cellular and molecular mechanism.
Activity-dependent neuronal tagging and single-cell profiling
We identify and compare experience-linked cells and their molecular programs.
High-density recording and closed-loop circuit control
Silicon probes, optotagging, and closed-loop optogenetics connect population dynamics to causal tests.
Whole-cell physiology and circuit mapping
Patch-clamp measurements plus local and long-range tracing link circuit activity to synaptic and cellular mechanisms.
Multiscale integration
We combine systems, cellular, and molecular measurements to follow a single question across levels of organization.