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June 2004 Vol 5 No 6 HIGHLIGHTS
Nature Reviews Neuroscience 5, 429 (2004); doi:10.1038/nrn1414
[535K]
LEARNING AND MEMORY
Re-making memories
Rachel Jones
There is increasing evidence that stable memories need to be
'reconsolidated' after being retrieved, and that this process has some
features in common with the initial consolidation of long-term memories --
for example, both require protein synthesis. But now, writing in Science, Lee
et al. have shown that consolidation and reconsolidation in the hippocampus
involve different cellular processes
The type of memory that the authors studied is
contextual fear conditioning. When a rat is
placed in a chamber and given a footshock, it
immediately becomes conditioned to associate
the chamber with the shock. On a later test,
when the rat is placed in the chamber, it will
show freezing behaviour, and this can be
quantified as a measure of learning. This type of
learning depends on the hippocampus, and has
been widely used in the study of consolidation
and reconsolidation.
Lee and colleagues used antisense
oligodeoxynucleotides to investigate the roles of
brain-derived neurotrophic factor (BDNF) and
the transcription factor Zif268 in the
consolidation and reconsolidation of fear conditioning. Antisense
oligodeoxynucleotides work by inhibiting the expression of a specific protein
at the site of infusion. When BDNF antisense oligodeoxynucleotides were
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infused into the hippocampus 90 min before the training session, the rats
showed normal freezing behaviour when tested after 3 h, indicating that
they had learned the fear conditioning and stored it normally in short-term
memory. However, when tested after 24 h, their memory was impaired,
showing that the BDNF antisense had prevented the consolidation of the
experience into long-term memory.
When the rats are tested by being placed in the chamber but not shocked,
their freezing behaviour shows that they are retrieving the memory that was
formed after training. Inhibition of protein synthesis at this point prevents
the memory from being reconsolidated, so that on subsequent tests the rats
show reduced freezing. Infusion of BDNF antisense into the hippocampus
before testing did not prevent reconsolidation -- unlike the initial
consolidation, reconsolidation of the fear memory does not require the
generation of BDNF in the hippocampus. However, when the authors infused
a Zif268 antisense oligodeoxynucleotide into the hippocampus before
testing, reconsolidation was impaired.
In fact, there was a neat double dissociation. Not only was BDNF required
for consolidation but not reconsolidation; in addition, Zif268 was required
for reconsolidation but not for consolidation. This is a convincing
demonstration that the two processes involve different (although potentially
overlapping) cellular mechanisms, and should open the way for a clearer
understanding of both.
References and links
ORIGINAL RESEARCH PAPER
Lee, J. L. C. et al. Independent cellular processes for hippocampal memory
consolidation and reconsolidation. Science 304, 839­843
(2004) | Article | ChemPort |
FURTHER READING
Nadel, L. & Land, C. Memory traces revisited. Nature Rev. Neurosci. 1, 209­
212 (2000) | Article | PubMed | ISI | ChemPort |
Millin, P. M. et al. Interpretations of retrograde amnesia: old problems
redux. Nature Rev. Neurosci. 2, 68­70 (2001) | Article
| PubMed | ISI | ChemPort |
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 2004 Nature Publishing Group
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