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New protein synthesis not essential to memory formation
Diana Yates, Life Sciences Editor
photo to enlarge
by L. Brian Stauffer
Paul E. Gold and colleagues have demonstrated that
new protein synthesis is not required for long-term
memory formation, a discovery that challenges basic
assumptions about the mechanisms of memory.
Ill. — New research from the University of Illinois
challenges the premise that the brain must build new proteins in response
to an experience for that experience to be recorded in long-term memory.
The findings, published in the Proceedings of the National Academy
of Sciences, could alter basic assumptions about the role of protein
synthesis in memory formation.
Brain researchers have long used drugs that enhance or hinder memory
formation to gain insight into the mechanisms at play. Early experiments
in rats found that protein synthesis inhibitors injected into brain
regions involved in memory processing could disrupt long-term memory
formation. This led some to hypothesize that new protein synthesis
was essential to the creation of long-term memories.
A research team led by neuroscientist Paul E. Gold discovered an alternate
explanation for this effect. The researchers observed that the protein
synthesis inhibitor anisomycin, which is commonly used in memory studies,
causes dramatic changes in brain chemistry – apart from protein
synthesis inhibition – that interfere with memory formation.
They found that exposing rat brains to anisomycin sets off wild fluctuations
in neurotransmitter levels in the brain region targeted in the experiment – the
amygdala, one of several brain structures involved in processing memories
and emotions. Large fluctuations in neurotransmitter levels in the
amygdala are known to interfere with memory formation.
The researchers were surprised by the intensity of the brain’s
response to anisomycin. Shortly after they injected the drug into the
rat amygdala, they saw huge increases – from 1,000 to 17,000
percent – in levels of the neurotransmitters norepinephrine,
dopamine and serotonin.
“This is far above anything we’ve seen physiologically in any experiment,” Gold
said. “Normally you think of a 200 percent increase as a really solid
result and 300 percent as outrageously high. I wouldn’t have thought
that there was that much (neurotransmitter) to be released.”
Shortly after this spike, dopamine and norepinephrine levels plummeted,
dropping well below baseline for up to 48 hours after the initial exposure
As expected, the rats exposed to anisomycin prior to training had impaired
long-term recall of the events. To determine whether the inability
to form lasting memories was caused by the anisomycin or by changes
in neurotransmitter levels, the researchers repeated the experiment,
adding drugs designed to counter the fluctuations in neurotransmitter
levels. When the neurotransmitter imbalances were neutralized or blunted – even
in the presence of anisomycin – memory formation was significantly
“If we block anisomycin’s effects on the neurotransmitters, then
we block many of its effects on memory,” Gold said. “We still have
the protein synthesis inhibition, but it no longer causes the (same level of)
It is possible that some of the amnesia is due to the cessation of
protein synthesis, Gold said. But, he said, the evidence suggests otherwise. “I
think the protein synthesis inhibition itself is causing cells to act
in unusual ways,” he said.
“No one would deny that protein synthesis is needed to maintain normal
brain functions, including memory,” Gold said. “But the idea that new protein
synthesis is required to make long-lasting memories should be reexamined.”
Gold is a professor of psychology and psychiatry and is affiliated
with the neuroscience program and the Institute
for Genomic Biology.
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