Subicular plateaus signal reward locations during goal-directed Behavior

Here, we studied how the hippocampus communicates learned information to the rest of the brain. Using in vivo whole-cell recordings in behaving mice, we found that bursts of activity in subiculum neurons are often driven by sustained electrical events initiated in the dendrites called plateau potentials, which are shaped by synaptic input and NMDA receptor activation. Importantly, the cell’s internal state determines whether these events signal reward-related locations, revealing how single-neuron dynamics help organize learning-related output signals.

Learning-dependent feedback by OLM interneurons shapes CA1 representations

This research investigates how the brain forms internal maps of space during learning. Using two-photon Ca2+ imaging and bidirectional optogenetic manipulations, we show that a specific type of inhibitory neuron in the hippocampus helps regulate when and where new spatial representations are formed by controlling learning-related synaptic plasticity (BTSP). These findings reveal an important feedback mechanism that shapes how experiences are encoded into memory. 

Entorhinal cortex directs learning-related changes in CA1 representations

This work addresses the long-standing question of what neural mechanisms underlie learning within the mammalian brain. We show that a form of synaptic plasticity (BTSP) we discovered recently is responsible for the adaptive changes that occur in hippocampal area CA1 population activity as an animal learns a simple task.  We also present evidence that the EC3 is the source of a target-like instructive signal that drives BTSP to achieve a desired CA1 population activity.  

Inhibitory suppression of heterogeneously tuned excitation enhances spatial coding in CA1 place cells

We showed that synaptic inhibition greatly contributes to the sparse structure of the CA1 place cell activity by controlling for the relatively broadly tuned excitation that CA1 receives from its afferent brain areas. In particular, the spatially localized fields of place cell firing (‘place fields’) emerge from the interaction of a localized increase in synaptic excitation with spatially uniform inhibition. 

Behavioral time scale synaptic plasticity underlies CA1 place fields

We identified a new form of synaptic plasticity, called behavioral timescale synaptic plasticity (BTSP). This synaptic learning rule is driven by dendritic plateau potentials, with only a single plateau being sufficient to modify the strength of those synapses that are active in a seconds-long time window around the plateau. BTSP provides a mechanism for single-trial learning and could allow neurons to compute an association between an event and a delayed outcome, offering a solution to the long-standing ‘temporal credit assignment’ problem. 

NMDA receptor-receptor dependent multidendrite Ca2+ spikes required for hippocampal burst firing in vivo

We showed that a specific type of dendritic Ca2+ spike, Ca2+ plateau potentials (‘plateaus’ for short), underlies burst firing of CA1 neurons in vivo. These were the first simultaneous in vivo whole-cell and two-photon dendritic Ca2+ recordings in CA1 neurons. 

*Preview article in Neuron by Thomas Oertner 

Staged decline of neuronal function in vivo in an animal model of Alzheimer’s Disease 

We showed that pyramidal cells in the visual cortex of mice that mimic the neuropathological and behavioral features observed in Alzheimer’s disease exhibit an altered input-output relationship. This work indicates that restoring this transformation to the baseline state pharmacologically might be beneficial for patients.

Sound-evoked network calcium transients in mouse auditory cortex in vivo 

We recorded population calcium signals in the auditory cortex of mice using fiber photometry. We found that these slow 1s - long sensory‐evoked network calcium transients (NCaT) are related to global ‘up states’ measured by electrocorticography and can be initiated by optogenetic activation of layer 5 pyramidal neurons, implying an intracortical mechanism for the initiation of the slow NCaTs.