CHAMPAIGN, Ill. -- A protein known primarily for its role in killing cells also plays a part in memory formation, researchers at the University of Illinois at Urbana-Champaign report. Their work exploring how zebra finches learn songs could have implications for treatment of neurodegenerative conditions such as dementia and Alzheimer's disease.

When activated, the enzyme caspase-3 triggers a synaptic process essential for memory storage, according to Graham R. Huesmann and David F. Clayton of the department of cell and developmental biology and of the U. of I. Beckman Institute for Advanced Science and Technology. Their article, which appears in the Dec. 21 issue of the journal Neuron, describes their findings, which provide "the first direct evidence of a change in the availability of activated caspase-3 protein in the brain during the process of memory formation."

Caspase-3 is best known for its role in a biochemical cascade that leads to apoptotic cell death. These new findings demonstrate that the enzyme acts differently under different conditions, and suggest that its regulation in the brain is more complex than previously thought. Huesmann and Clayton examined the brains of zebra finches after exposing the birds to tape recordings of the songs of other birds. They found an increase in the concentration of activated caspase-3 in post-synaptic sites of the auditory forebrain shortly after the birds were exposed to unfamiliar bird songs. Exposure to familiar songs caused no significant increase in the enzyme.

The researchers demonstrated that the activated form of caspase-3 is short-lived and highly localized, which may explain why the enzyme does not trigger apoptosis.

They also showed that activated caspase-3 is always present in brain cells, but that it is usually bound by an inhibitor, BIRC4. For a short time after the birds are exposed to novel songs, the inhibitor releases the activated caspase-3. The concentration of
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Contact: Diana Yates
diya@uiuc.edu
217-333-5802
University of Illinois at Urbana-Champaign
21-Dec-2006