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Boosting the function of a learning protein jams the brain with too much information, according to Ype Elgersma (Erasmus MC, Rotterdam, Netherlands), Alcino Silva (University of California, Los Angeles, CA), and colleagues. The result is a cautionary tale for those seeking to develop learning drugs.
A mouse with active αCaMKII is first to the target, but its learning is less flexible and less fine-tuned.
Elgersma
The team created mice lacking two inhibitory phosphorylation sites on αCaMKII. Wild-type αCaMKII is displaced from synapses in part by the phosphorylation, but the mutant protein has an enhanced affinity for synapses. This lowers the threshold for establishing long-term potentiation (LTP)—a synapse-strengthening event associated with learning—probably because it now takes less calcium rushing into the synapse to reach the necessary level of αCaMKII activity.
Initial water-maze learning by the mice was normal. But the mutant mice, unlike wild type, did...
The Rockefeller University Press
2002
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