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Protein that kills cells also
important for memory
Diana Yates,
Life Sciences Editor
217-333-5802; diya@illinois.edu
Released
12/20/06
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Click
photo to enlarge |
Photo
by L. Brian Stauffer |
| David
F. Clayton, left, and Graham R. Huesmann have studied
how zebra finches learn songs, which could have
implications for the treatment of neurodegenerative
conditions such as dementia and Alzheimer's disease. |
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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.
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Click
photo to enlarge |
Photo
by Sarah London |
| Male
zebra finch flanked by two females. |
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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 unbound, activated caspase-3
peaks about 10 minutes after the birds hear the new songs.
Other research has added to the evidence that caspase-3 is essential
to memory formation. Caspase-3 inhibitors injected into rat brains
interfere with the animals’ spatial memory and active avoidance
learning.
Caspase-3’s dual role as a cell killer and memory builder has
long intrigued Huesmann, the lead author of the study. “Is it
Memory or Is It Death? Caspase-3 and Memory Formation,” was his
dissertation title. Huesmann has a doctorate in neuroscience and is
completing a medical degree at Illinois.
“Graham had this intuition that growth and memory is really a
kind of remodeling,” said Clayton, who is a professor of cell
and developmental biology. “You can’t have growth without
death.”
Editor’s note: To reach Graham R. Huesmann,
call 217-244-1450; e-mail: huesmann@illinois.edu.
To reach David F. Clayton, call 217-244-3668; e-mail: dclayton@illinois.edu.
