Research in the Blitzer Laboratory addresses the mechanism of memory formation through the phenomenon of synaptic plasticity. In particular, we are interested in a persistent form of increased synaptic efficiency, termed long-term potentiation (LTP), which can be induced in the hippocampus, a brain structure concerned with memory formation and retrieval. LTP is induced by physiological stimulation, and is a highly regulated process involving numerous signaling pathways. Current projects include:

1) The detailed analysis of the roles of signaling pathways in LTP induction. This is a broad topic, and includes such topics as interactions between MAP kinase and Ca2+/calmodulin kinase II and the inhibition of protein phosphatases by the cAMP pathway.

2) The mechanism of LTP maintenance. Memories tend to be persistent, but the correspondingly persistent phase of LTP remains relatively unexplored. The underlying processes are only beginning to be understood, but are clearly different from those of LTP induction. We are gaining insight into maintenance processes using manipulations, both physiological and pharmacological, that can reverse well-established LTP.

3) The synaptic locus of LTP. LTP induction requires both presynaptic and postsynaptic events. However, a major unresolved issue in the field is whether the expression of LTP reflects a pre- or postsynaptic change. A presynaptic change might be increased glutamate release, while postsynaptic possibilities include recruitment of new glutamate channels to the membrane and regulation of existing receptors phenomenon. We are using quantal analysis methods to address this issue.

Most of our projects are collaborative and interdisciplinary in design, including biochemical, molecular biological, and imaging techniques in addition to the lab's core expertise in neurophysiology.

LTP, memory, neurophysiology, hippocampus, signaling