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Monday, January 21, 2013
Accepted Memory Formation Model Refuted
This is a neat bit of science that clearly shows us that the working
hypothesis simply does not work. Implied in all that is that
repetition is effects memory formation when that would be quite an
inefficient protocol. Why not infer instead that the mind makes a
specific decision to retain a memory point which can then be over
ridden by further work? Do not infer that this process is passive
That certainly explains the plasticity of memory. In my own case I
have observed my own mind balking at actual memorization of any kind
whenever I tried to retain apparent nonsense. Yet if I choose to note
something and I determine a need much later for that item, my memory
becomes clear as glass. It really impresses folks when you reference
an item read or a lecture comment from decades ago.
I have also noted that my mind also balks learning a mathematical
proof that is flawed. A rather handy trick when working on new
ideas or mushy old ideas. Think about this and then test your own
mind to see if it works for you.
Bye the bye. A perfect memory allows you to know and believe every
error produced by mankind while lacking sufficient skills to
understand this. The process of remembering these errors naturally
firmly embedded them in your mind making it almost impossible to
change your thinking. Thus the majority of scholars who naturally
depended on powerful memories are usually trapped by their own
A study by Johns
Hopkins researchers has shown that a widely accepted model of
long-term memory formation - that it hinges on a single enzyme in the
brain - is flawed. The new study, published in Nature, 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.
theory is that when you learn something, you strengthen connections
between your brain cells called synapses," explains Richard
Huganir, Ph.D., a professor and director of the Johns Hopkins
University School of Medicine's Department of Neuroscience.
"The question is,
how exactly does this strengthening happen?"
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," says Lenora Volk, Ph.D., a
member of Huganir's team. "We thought that learning the enzyme's
target could tell us a lot about how memories are stored and
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." The
brains of the mice without PKM-zeta were indistinguishable from those
of other mice, she says.
synapses of the PKM-zeta-less mice responded to the memory-erasing
ZIP molecule just as the synapses of normal mice do.
The team then
considered whether, in the absence of PKM-zeta, the mouse brains had
honed a substitute synapse-building pathway, much in the way that a
blind person learns to glean more information from her other senses.
So the researchers
made mice whose PKM-zeta genes functioned normally until they were
given a drug that would suddenly shut the gene down.
This allowed them to
study PKM-zeta-less adult mice that had had no opportunity to develop
a way around the loss of the gene. Still, the synapses of the
so-called conditional knockout mice responded to stimuli just as
synapses in normal mice did.
What this means, the
researchers say, is that PKM-zeta is not the key long-term memory
molecule previous studies had suggested, although it may have some
role in memory.
"We don't know
what this ZIP peptide is really acting on," says Volk. "Finding
out what its target is will be quite important, because then we can
begin to understand at the molecular level how synapses strengthen
and how memories form in response to stimuli."
Other authors on the
paper are Richard Johnson and Yilin Yu, both of the Johns Hopkins
University School of Medicine.
This study was
supported with funds from the National Institute of Neurological
Disorders and Stroke (grant number NS36715), the National Institute
of Mental Health (grant number T32MH15330) and the Howard Hughes