Experts refute accepted model of memory formation
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In a new study, researchers have shown that a widely accepted model of long-term memory formation — that it hinges on single enzyme in the brain — is flawed.
The new study by Johns Hopkins researchers found that mice lacking the enzyme that purportedly builds memory were in fact still able to form long-term memories as well as normal mice could.
"The prevailing theory is that when you learn something, you strengthen connections between your brain cells called synapses," Richard Huganir said.
"The question is, how exactly does this strengthening happen?" he said.
A research group at SUNY Downstate, led by Todd Sacktor, Ph.D., has suggested that key to the process is an enzyme they discovered, known as PKM-zeta. In 2006, Sacktor's group made waves when it created a molecule that seemed to block the action of PKM-zeta — and only PKM-zeta.
When the molecule, dubbed ZIP, was given to mice, it erased existing long-term memories. The molecule caught the attention of reporters and bloggers, who mused on the social and ethical implications of memory erasure.
But for researchers, ZIP was exciting primarily as a means for studying PKM-zeta.
"Since 2006, many papers have been published on PKM-zeta and ZIP, but no one knew what PKM-zeta was acting on," Lenora Volk, a member of Huganir's team, said.
"We thought that learning the enzyme's target could tell us a lot about how memories are stored and maintained," Volk said.
For the current study, Volk and fellow team member Julia Bachman made mice that lacked working PKM-zeta, so-called genetic "knockouts". The goal was to compare the synapses of the modified mice with those of normal mice, and find clues about how the enzyme works.
But, says Volk, "What we got was not at all what we expected. We thought the strengthening capacity of the synapses would be impaired, but it wasn't."
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