The study, which will appear in the Feb. 6 issue of the journal Cell, has broad implications for our understanding of how learning and memory normally occur, and how these abilities may be undermined in psychiatric and neurologic diseases.
Long-lasting memories are stored in the brain through strengthening of the connections, or synapses, between neurons. Researchers have known for many years that neurons must turn on the synthesis of new proteins for long-term memory storage and synaptic strengthening to occur, but the mechanisms by which neurons accomplish these tasks have remained elusive.
The MIT research team, led by Nobel laureate Susumu Tonegawa, director of the Picower Center for Learning and Memory, has now identified a crucial molecular pathway that allows neurons to boost their production of new proteins rapidly during long-term memory formation and synaptic strengthening.
"What we have discovered that hasn't been established before is that there is a direct activational signal from the synapse to the protein synthesis machinery," said Tonegawa, the Picower Professor of Biology and Neuroscience MIT's Departments of Brain and Cognitive Sciences and Biology. The central component of this pathway, an enzyme called "mitogen-activated protein kinase" (MAPK), effectively provides a molecular switch that triggers long-term memory storage by mobilizing the protein synthesis machinery.
Acting on a hunch that MAPK might be an important part of such a "memory switch," Ray Kelleher, a postdoctoral fellow in Tonegawa's laboratory and lead author of the study, created mutant mice in which the function of MAPK was selectively inactivated in the adult brain. In
Contact: Elizabeth Thomson
Massachusetts Institute of Technology