Todd C. Sacktor is Distinguished Professor of Physiology & Pharmacology, Anesthesiology, and Neurology at SUNY Downstate Medical Center. He received an A.B. from Harvard College in 1978, and an M.D. with Distinction for Research in Neuroscience from the Albert Einstein College of Medicine in 1982. After a residency in Neurology at Columbia Presbyterian Medical Center, he studied the role of protein kinase C (PKC) in short-term memory using the model system Aplysia californica, in the laboratory of Dr. James H. Schwartz, at the Center for Neurobiology and Behavior, directed by Dr. Eric R. Kandel. In his own laboratory at SUNY Downstate in 1990, he discovered a brain-specific PKC isoform, PKMzeta. Together with colleagues, his laboratory demonstrated that PKMzeta was both necessary and sufficient for maintaining long-term potentiation (LTP) and storing the long-term memory trace.
In this time of troubles, there are many memories we would like to forget. To root out a traumatic memory completely, we have to understand the biological basis of memory, itself.
Over several decades, neuroscientists have learned much about how long-term memories are initially formed. When an experience is to be remembered, groups of nerve cells, maybe a few thousand, start to fire simultaneously. Nerve cells are connected by synapses, and when the connected cells fire at the same time, the synapses between them become persistently strengthened, forming a network of cells. When a memory is in storage, the cells don’t fire, but the strengthened connections between them persist.
Until recently, almost nothing was known about this persistent synaptic strengthening process. But over the last few years, our laboratory has spearheaded the discovery of a unique, persistently active molecule, an enzyme termed PKMzeta, that is formed during learning and maintains the strength of the synaptic connections. Remarkably, in experimental animals, inhibiting PKMzeta with drugs erases prior long-term memories, without otherwise damaging the brain, or, once the drug has washed out, preventing new memories from forming. But because PKMzeta is a general mechanism for memory storage, inhibiting the enzyme results in an amnesia for most if not all long-term memories. Currently, we and other labs around the world are taking advantage of our growing knowledge about how this fundamental memory mechanism works to disrupt the specific PKMzeta molecules that maintain traumatic memories.