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| Monterotondo, 8 January 2007 |
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| Getting to the bottom of memory
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Liliana Minichiello at the EMBL Mouse Biology Unit in Monterotondo, Italy. |
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For the first time researchers investigate the molecular basis of memory in
living mice
Italiano
Press
Release 8 January 2007 [PDF]
Phone numbers, the way to
work, granny's birthday – our brain with its finite number of
nerve cells can store incredible amounts of information. At the
bottom of memory lies a complex network of molecules. To
understand how this network brings about one of the most
remarkable capacities of our brain we need to identify its components
and their interactions. Researchers from the European
Molecular Biology Laboratory's [EMBL] Mouse Biology Unit in
Monterotondo, Italy, and the Universidad Pablo de Olavide in
Sevilla, Spain, now for the first time investigate the molecular
basis of memory in living mice. The study, which appears in the
current issue of Learning and Memory, identified a molecule that
is crucially involved in learning and singled out the signaling
pathway through which it affects memory.
Our sense organs inform our brain about what happens around
us and brain cells communicate this information between each
other using electrical signals. These signals become stronger the
more often a cell experiences the same stimulus, allowing it to distinguish
familiar information from news. In other words, a cell
remembers an event as an unusually strong and long-lasting signal.
This phenomenon called long-term potentiation [LTP] is
thought to underpin learning and memory and its molecular
basis is being investigated intensively.
"It is difficult to study a dynamic process like memory in the test
tube," says Liliana Minichiello, whose group carried out the study
at EMBL's Mouse Biology Unit in collaboration with Agnès
Gruart at the Universidad Pablo de Olavide in Sevilla, Spain, who
performed the behavior and in vivo recordings. "To assess if the
molecular mechanisms that generate LTP also underpin memory
formation you need to study a living animal while it is learning."
Minichiello and her team combined molecular, electrophysiological
and behavioural methods in a sophisticated mouse model.
This new approach allowed them for the first time to start dissecting
the molecular basis of LTP while simultaneously addressing
effects on learning and memory. Using genetic methods they generated
mouse strains with a defective version of a receptor molecule
called TrkB. TrkB is found on the surface of cells in the hippocampus,
an area of the brain involved in memory formation,
and translates incoming signals into cellular responses. Mice with
the defective TrkB, which is incapable to activate an important
signaling pathway involving the protein PLCγ, were no longer
able to learn. At the same time the LTP that normal hippocampal
cells generate in response to familiar stimuli was abolished.
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TrkB and the PLCγ activated signaling pathway are central to
both LTP and learning. For the first time we have been able to
prove that LTP and learning do in fact have a common molecular
basis," says José Delgado-García from the University of Sevilla.
For the future Minichiello and her lab are aiming to gain an even
better understanding of TrkB and its role in learning and memory.
Their research might give new impulses also to studies concerned
with human memory, because underlying molecular pathways
are likely to be conserved between species.
Source Article
A. Gruart, C. Sciaretta, M. Valenzuela-Harrington, J. Delgado-García & L. Minichiello et al., Mutation at the TrkB PLCγ-docking site
affects hippocampal LTP and associative learning in mice, Learning and Memory, 8 January 2007
Press Contact
Anna-Lynn Wegener
Press Officer
EMBL Heidelberg
Tel: +49 6221 387-8452
Email: wegener@embl.de |
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