Our daily experience can trigger lasting memories, which are stored in our brains. Memories are stored ultimately by changing the way neurons convey information. More precisely, they are stored as changes in the function of synapses: the structures by which neurons contact and transmit signals to each other. My laboratory is interested in exploring the cellular and molecular changes that happen at the synapses to allow memory storage.

Combining various techniques, such as electrophysiological recording, biochemical/molecular analysis, and imaging, we are aiming to understand the cellular and molecular changes that happen during synaptic plasticity. It is well established that neural activity can trigger synaptic changes, such as long-term potentiation (LTP) and long-term depression (LTD), which are cellular models of learning and memory. Currently we are looking at postsynaptic mechanisms of LTP and LTD. We found that synaptic plasticity is associated with changes in postsynaptic glutamate receptors. LTP and LTD are associated with changes in phosphorylation of the GluR1 subunit of AMPA type glutamate receptors. Using genetically altered mice that lack phosphorylation sites on GluR1, we found that LTP and LTD are both impaired. One line of research involves elucidating the downstream events that follow AMPA receptor phosphorylation changes.

In addition to understanding the basic mechanisms of memory formation, we are also interested in elucidating the events that occur in diseased brains. Alzheimer's disease is a devastating memory disorder that affects the social well-being of affected individuals. In collaboration with Dr. Philip Wong at Johns Hopkins School of Medicine, we are analyzing various mouse models of Alzheimer's disease, especially focusing on the possible alterations in synaptic plasticity mechanisms.