First Evidence That Neurons Need To
Erase Old Memories To Make Room For New Ones
Short-term memory may depend in a surprising way on the ability
of newly formed neurons to erase older connections. That's the
conclusion of a report in the November 13th issue of the journal
Cell, a Cell Press publication, that provides some of the first
evidence in mice and rats that new neurons sprouted in the hippocampus
cause the decay of short-term fear memories in that brain region,
without an overall memory loss.
The researchers led by Kaoru Inokuchi of The University of Toyama
in Japan say the discovery shows a more important role than many
would have anticipated for the erasure of memories. They propose
that the birth of new neurons promotes the gradual loss of memory
traces from the hippocampus as those memories are transferred
elsewhere in the brain for permanent storage. Although they examined
this process only in the context of fear memory, Inokuchi says
he "thinks all memories that are initially stored in the
hippocampus are influenced by this process."
In effect, the new results suggest that failure of neurogenesis
will lead to problems because the brain's short-term memory is
literally full. In Inokuchi's words, we may perhaps experience
difficulties in acquiring new information because the storage
capacity of the hippocampus is "occupied by un-erased old
Of course, Inokuchi added, "our finding does not necessary
deny the important role of neurogenesis in memory acquisition."
Hippocampal neurogenesis could have a dual role, he says, in both
erasing old memories and acquiring new ones.
Earlier studies had shown a crucial role for the hippocampus
in memorizing new facts. Studies in people with impaired and normal
memories and in animals also showed that information recall initially
depends on the hippocampus. That dependence progressively decays
over time as memories are transferred to other regions, such as
the neocortex. Scientists have also observed a similar decay in
the strength of connections between neurons of the hippocampus,
a phenomenon known as long-term potentiation (LTP) that is considered
the cellular basis for learning and memory.
Scientists also knew that new neurons continue to form in the
hippocampuses of adults, even into old age. But it wasn't really
clear what those newborn brain cells actually do. Inokuchi's team
suspected that the integration of new neurons was required to
maintain neural connections, but they realized it might also go
the other way. The incorporation of new neurons into pre-existing
neural circuits might also disturb the structure of pre-existing
information, and indeed that is what their new findings now show.
The researchers found that irradiation of rat's brains, which
drastically reduces the formation of new neurons, maintains the
strength of neural connections in the hippocampus. Likewise, studies
of mice in which hippocampal neurogenesis was suppressed by either
physical or genetic means showed a prolonged dependence of fear
memories on that brain region.
On the other hand, voluntary exercise, which causes a rise in
the birth of new neurons, sped up the decay rate of hippocampus-dependency
of memory, without any memory loss.
"Enhanced neurogenesis caused by exercise may accelerate
memory decay from the hippocampus and at the same time it may
facilitate memory transfer to neocortex," Inokuchi said.
"Hippocampal capacity of memory storage is limited, but in
this way exercise could increase the [brain's overall] capacity."
The study sets the stage for further examination of the connections
between neurogenesis and learning capacity, the researchers say.
They also plan to examine how the gradual decay of memory dependence
on the hippocampus relates to the transformation of memory over
time from a detailed and contextually-rich form to a more generic
Reference Source 128
November 13, 2009