Protein believed to control formation of memory identified by Scripps & UCSD ...( of DNA and protein called chromatin. T...)

But when a gene is going to be expressed, such as during the formation of long-term memory, the chromatin must be opened up and the DNA unwound from the histones. CBP plays a critical role in this process because it acetylates amino acids known as lysine on the histones, and this makes the histones lose their affinity for the DNA and facilitates the expression of genes on that DNA.

Losing and Regaining Memory Ability

Korzus and Mayford performed an experiment in which they could turn on a defective form of CBP in adult rodents. They found that the defective CBP cannot acetylate the histones, and this prevents the DNA wound around the histones from releasing. This, in turn, prevents protein synthesis, and that prevents the formation of long-term memory.

Significantly, Korzus and Mayford were able to correct the long-term memory defect in the animals by administering a leukemia drug called histone deacetylase inhibitor Trichostatin A, which put the acetyl group back on the histones.

Their results suggest that remodeling of chromatin is important in learning and memory. It also provides a new mechanism for influencing cognitive function. And it suggests a possible treatment for the mental retardation associated with Rubinstein-Taybi syndrome.

The article, "CBP histone acetyltransferase activity is critical component of memory consolidation" by Edward Korzus, Michael G. Rosenfeld, and Mark Mayford appears in the June 24, 2004 issue of the journal Neuron. See http://www.neuron.org.

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Contact: Jason Bardi
jasonb@scripps.edu
858-784-9254
Scripps Research Institute
23-Jun-2004