John Lisman, Ph.D.
Professor, Biology Department and
Volen National Center for Complex Systems and
Chair, Neuroscience Program
Brandeis University
Waltham, Massachusetts
CaMK11 as a Synaptic Memory
Molecule: the Final Key Experiments Fall Into Place
An important unsolved problem in Neuroscience is the
molecular basis of memory. This problem is being extensively
studied in many laboratories using LTP of hippocampal
synapses as a model system. In this LTP model, synapses
are briefly stimulated with high frequency stimulation.
As a result, they undergo a persistent strengthening that
can last for years. Dr. Lisman has been investigating
the molecular basis of this strengthening. Considerable
evidence has accumulated for a role for the protein kinase,
CaMKll, in this process. This kinase is persistently activated
after LTP. Moreover, when introduced into neurons it can
potentiate synapses in a way that occludes with LTP. They
have now investigated whether the persistent activation
of CaMK11 has a role in the persistence of LTP. He finds
that application of a CaMK11 inhibitor can reverse saturated
LTP. Importantly, after such reversal, additional LTP
can be induced. Taken together with previous work, these
results make a strong case for CaMK11 as a key molecule
underlying synaptic memory.
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