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Synapses are the fundamental nodes of information transmission in the brain. Activity-dependent changes in the efficacy of synaptic transmission, called synaptic strength, are crucial for how the brain perceives and reacts to the environment, learns and stores memories. The highly diverse synaptic strengths found in neural circuits may reflect the on-going information coding and adaptive processes associated with executing brain functions.

 Our laboratory uses the rodent hippocampus as the model system. Focusing on the main excitatory neurons of specific hippocampal connections and starting from the properties of individual synapses, we assess their interactions with neighboring synapses in shaping the population activity that supports hippocampal circuit functions.

 Different forms of synaptic plasticity operate in concert. For example, Hebbian plasticity, representing cellular forms of learning, is thought to engage compensatory, homeostatic plasticity in order to maintain synaptic circuits within their functional range. How individual synaptic strengths are set and controlled across a synapse population and the cellular and the molecular basis by which synaptic strength diversity arises remain to be clarified. We take a bottom-up approach to address the basic principles underlying synaptic circuit functions, using a combination of the techniques of cell and molecular biology, live and ultrastructural imaging, and electrophysiology, and validate the physiological significance in behaving mice.

Ongoing projects include: Delineating the nature of input-specificity and synaptic competition by examining activity-dependent distribution of pre- and postsynaptic strengths across dendrites of single CA1 neurons;

Studying a hidden role for astrocytes in regulating synaptic strength diversity in CA1 neurons by characterizing astrocyte organization and signaling; assessing the physiological impact of such mechanisms;

Exploring how adhesion proteins contribute to axonal compartmentalization and synapse specificity;

Studying the homeostatic synaptic regulation of the DG-CA3 network and how its dysfunction might contribute to changes in anxiety-like behaviors.