Research in the Glowatzki Lab focuses on the auditory system, with a particular focus on synaptic transmission in the inner ear. Our lab is using dendritic patch clamp recordings to examine mechanisms of synaptic transmission at this first, critical synapse in the auditory pathway. With this technique, we can diagnose the molecular mechanisms of transmitter release at uniquely high resolution (this is the sole input to each afferent neuron), and relate them directly to the rich knowledge base of auditory signaling by single afferent neurons. We study pre- and post-synaptic mechanisms that determine auditory nerve fiber properties. This approach will help to study general principles of synaptic transmission and specifically to identify the molecular substrates for inherited auditory neuropathies and other cochlear dysfunctions.

The Laboratory of Richard L. Huganir is interested in the mechanisms that regulate synaptic transmission and synaptic plasticity. Our general approach is to study molecular and cellular mechanisms that regulate neurotransmitter receptors and synapse function. We are currently focusing our efforts on the mechanisms that underlie the regulation of the glutamate receptors, the major excitatory neurotransmitter receptors in the brain.

The Lau Lab uses a combination of computational and experimental approaches to study the atomic and molecular details governing the function of protein complexes involved in intercellular communication. We study ionotropic glutamate receptors (iGluRs), which are ligand-gated ion channels that mediate the majority of excitatory synaptic transmission in the central nervous system. iGluRs are important in synaptic plasticity, which underlies learning and memory. Receptor dysfunction has been implicated in a number of neurological disorders.

The Hey-Kyoung Lee Lab is interested in exploring the cellular and molecular changes that happen at synapses to allow memory storage. We use various techniques, including electrophysiological recording, biochemical and molecular analysis, and imaging, to understand the cellular and molecular changes that happen during synaptic plasticity. Currently, we are examining the molecular and cellular mechanisms of global homeostatic synaptic plasticity using sensory cortices as model systems. In particular, we found that loss of vision elicits global changes in excitatory synaptic transmission in the primary visual cortex. Vision loss also triggers specific synaptic changes in other primary sensory cortices, which we postulate underlies sensory compensation in the blind. One of our main research goals is to understand the mechanisms underlying such cross-modal synaptic plasticity. We are also interested in elucidating the events that occur in diseased brains. In collaboration with other researchers, we are analyzing various mouse models of Alzheimer's disease, especially focusing on the possible alterations in synaptic plasticity mechanisms.