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Molecular basis for learning,
memory found in mice
By Candace Lombardi
Staff Writer, CNET News.com
Published: January 4, 2007, 9:00 PM PST
European
scientists have proved there is a shared molecular basis for
mice's ability to learn, form memories and recall them.
A cellular molecule in the brain's hippocampus is responsible,
according to a group led by Liliana Minichiello at the European
Molecular Biology Laboratory in Monterotondo, Italy, together
with Agnès Gruart from the Universidad Pablo de Olavide in
Spain.
"Obviously, mental illnesses can better be cured when you know
what molecules are involved. Right now, these drugs in
existence, they do something, but very little. And I think that
is because of a lack of knowledge about the molecular mechanism.
It is not the first target to make a drug, but (our discovery)
definitely will aid the people that do that work," said
Minichiello.
Scientists have long known that neurons in the brain communicate
via electrical signals. A particularly strong and long-lasting
signal to a brain cell is believed to be an indication of new
information. Long-term protentation (LTP), the term for this
phenomenon, is believed by scientists to be the origination of
learning and recall at the molecular level.
In order to study this process as it is happening, scientists
must be able to monitor the brain while it is learning.
Minichiello and her group were able to monitor mice while they
learned and recalled that new knowledge. Through this, the group
tested whether a receptor molecule called TrkB, which is found
in some hippocampus cells, may be central for the LTP process to
take place.
"Other studies in our lab said that this molecule was
significant. This went deeper and produced more evidence. We
measured the LTP while the mouse was conscious and learning. The
mouse was alive," Minichiello said.
Minichiello's group determined that mice with defective TrkB
molecules were unable to activate an important signaling
pathway, and were also unable to learn. In addition, they found
that the cells with defective TrkB molecules were unable to
generate a normal LTP recall response (remembering) when
presented with a familiar situation.
In other words, the ability to learn, and the ability to recall
something that had been learned, was impaired in mice without
healthy TrkB molecules.
"We
established that while the mouse is learning, there are changes
in the hippocampus that do not happen if you mutate the
receptor. It helps us to understand the molecular pathway for
learning, but also for generating LTP," Minichiello said.
The discovery is significant in that it is the first time
scientists have been able to prove that TrkB and the signaling
pathway it activates are essential to learning and memory,
according to Minichiello.
Full results of the group's finding will be published Friday in
the journal Learning and Memory.
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