A team of scientists has identified the existence of a back-up plan
for memory storage, which comes into play when the molecular mechanism
of primary long-term memory storage fails.
Previous work had shown that mice engineered without an enzyme
crucial to long-term memory storage could still form such memories,
creating a controversy that a team of scientists has now resolved with
the new research, which appears in the journal eLife.
The research focused on an enzyme made in nerve cells—PKMzeta. In a
series of experiments, they confirmed that while the enzyme is crucial
to long-term memory in normal mice, the mice engineered without PKMzeta
still form long-term memories because they deploy an alternative,
previously silent memory-storage method.
“Mice missing the PKMzeta enzyme essential for long-term memory are
able to recruit a back-up mechanism for long-term memory storage,”
explains André Fenton, a professor in NYU’s Center for Neural Science
and one of the paper’s co-authors. “The question now is: how does
PKMzeta function and what is the mechanism of its interaction with the
PKCiota/lambda backup mechanisms?”
Previous research has found PKMzeta plays an important role in
long-term memory storage, which scientists believe depends on the
persistent strengthening of the connections between nerve cells.
Specifically, the enzyme is made during the strengthening of these
connections, and it remains in place so long as the links remain strong.
Notably, studies examining the role of PKMzeta’s in memory found that
when the enzyme’s function was weakened in rodents,after they formed
long-term memory, the animals could no longer remember diverse types of
memories depending on diverse parts of the brain, suggesting that
PKMzeta is a general memory storage mechanism.
But, recently, the importance of PKMzeta was questioned by
experiments on genetically engineered “knockout” mice in which the gene
that makes PKMzeta was deleted. Without PKMzeta, the knockout mice could
still strengthen connections between nerve cells and still learn and
While some took these results as evidence that PKMzeta’s role had
previously been overstated, such studies did not consider the
possibility of a “back-up” mechanism for memory that takes over when
PKMzeta is removed. So the question remained: Is PKMzeta unimportant for
memory or, in its absence, is a back-up mechanism deployed?
To address this matter, Panayiotis Tsokas, a research professor in
Todd Sacktor’s lab at SUNY Downstate Medical Center, Fenton, and their
colleagues tested both the “PKMzeta is unimportant” and “PKMzeta is
compensated” hypotheses. To do so, they used a piece of modified DNA as a
drug to block the formation of PKMzeta. If another molecule or
molecules act as a back-up mechanism for PKMzeta, the scientists
reasoned, the new drug would block the formation of memory in normal
mice, but would have no effect on memory in the knockout mice that
cannot make PKMzeta — the drug would have nothing to work on.
The results supported the PKMzeta is compensated hypothesis—the
formation of memories normal mice was disrupted while that for the
knockout mice was not, confirming the importance of PKMzeta, but also
pointing to the presence of a back-up mechanism, which they identified
involves PKCiota/lambda, the most closely related molecule to PKMzeta.
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