[MURG] [>Htech] sciencedaily: abnormal cortex synapse shape impairs long term memory (fwd from alito@organicrobot.com)

[Eugen Leitl]

----- Forwarded message from Alejandro Dubrovsky <alito at organicrobot.com> -----

From: Alejandro Dubrovsky <alito at organicrobot.com>
Date: Sun, 20 Jun 2004 19:15:46 +1000
To: transhumantech <transhumantech at yahoogroups.com>
Subject: [>Htech] sciencedaily:  abnormal cortex synapse shape impairs long term
	memory
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(
http://web.mit.edu/newsoffice/2004/neuron.html
)

Synapse size and shape key in storing long-term memories
June 10, 2004

In a study to appear in the June 10 issue of Neuron, neuroscientists at
the Picower Center for Learning and Memory at MIT show for the first
time that storage of long-term memories depends on the size and shape of
synapses among neurons in the outer part of the brain, the cerebral
cortex.

This confirms what scientists have long suspected--that there are
physical places in the brain that are repositories for all our
knowledge, experience and memory. When an experience or a fact is
repeated enough or elicits a powerful emotional response, it shifts from
short- to long-term memory. It moves from the hippocampus, in the
innermost fold of the temporal lobe, to the brain?s outermost region,
the cortex, which controls higher functions like abstract thought and
speech. MIT researchers studied how structural and functional
alterations of synapses--physical and chemical connections among
neurons--in the cortex affect the animal?s ability to store long-term
memory.

The MIT research provides the first evidence that synaptic structure and
function in the cortex are critical for their long-term storage as
memories are transferred from the hippocampus to the cortex.

Mansuo L. Hayashi, research affiliate at the Picower Center; Susumu
Tonegawa, Director of the Picower Center and laureate of the 1987 Nobel
Prize; and colleagues at Johns Hopkins University and the Tata Institute
for Fundamental Research in India created mutant mice with abnormally
structured synapses in their cortexes. The synapses in their
hippocampuses were normal. "We showed their formation of memories is
fine," Hayashi said. "However, their long-term storage is impaired."

Like regular mice, the mutant mice were able to find their way around a
water maze in which they had to swim to a hidden platform with the help
of visual cues on the wall. Although mice can swim, they don?t like
water. The mutant mice learned the location of the platform, but after a
few weeks, they couldn?t remember where it was. The normal mice swam
right to it.

The work also provides insights into the memory deficits and cognitive
dysfunction in mentally retarded patients. Many of the genes tied to
mental retardation regulate the way synapses are formed. Abnormal
synapses apparently are responsible for the cognitive problems
associated with mental retardation.

PAK (p21-activated kinase), a critical regulator of synaptic
architecture, was inhibited in the mutant mice. In humans, the gene that
encodes this enzyme is tied to mental retardation. "Overall, we believe
that one of the underlying mechanisms for mental retardation is synaptic
malformation that leads to cognitive dysfunction," Hayashi said. "One of
the most significant findings of this study is that the structure of
synapses links to the function of synapses, and the size of synapses
reflect the strength of the synapse. The bigger the synapse, the more
vesicles to carry more neurotransmitters and the more channel proteins
to permeate and bind to the neurotransmitters."

In addition to Tonegawa, Hayashi and MIT research affiliate Hae-Yoon
Jung, authors include Se-Young Choi, Hey-Kyoung Lee, Dawai Zhang and
Alfredo Kirkwood at Johns Hopkins and B.S. Shankaranarayana Rao and
Sumantra Chattarji in India.

This work is supported by the National Institutes of Health, Howard
Hughes Medical Institute and RIKEN.




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