Penelitian begini sekarang ini lazimnya dibikin oleh orang kafir, di negeri 
kafir dan bukan di Kairo atau di Jeddah..  

Orang Islam sih lebih asyik zikir dan tunggang tunggik lima kali seharai atau 
saling berbunuhan karena alasan agama?? .. 

Islam itu, saya bilagn dan saya ulang adalahl aknat buat ummat manusia,a rtinya 
buat orang islamsendiri.

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  Web address:
     http://www.sciencedaily.com/releases/2008/10/
     081030123821.htm     
Scientists Identify Machinery That Helps Make Memories

ScienceDaily (Nov. 1, 2008) — A major puzzle for neurobiologists is how the 
brain can modify one microscopic connection, or synapse, at a time in a brain 
cell and not affect the thousands of other connections nearby. Plasticity, the 
ability of the brain to precisely rearrange the connections between its nerve 
cells, is the framework for learning and forming memories.

Duke University Medical Center researchers have identified a missing-link 
molecule that helps to explain the process of plasticity and could lead to 
targeted therapies.

The discovery of a molecule that moves new receptors to the synapse so that the 
neuron (nerve cell) can respond more strongly helps to explain several 
observations about plasticity, said Michael Ehlers, M.D., Ph.D., a Duke 
professor of neurobiology and senior author of the study published in the Oct. 
31 issue of Cell. "This may be a general delivery system in the brain and in 
other types of cells, and could have significance for all cell signaling."

Ehlers said this could be a general way for all cells to locally modify their 
membranes with receptors, a process critical for many activities -- cell 
signaling, tumor formation and tissue development.

"Part of plasticity involves getting receptors to the synaptic connections of 
nerve cells," Ehlers said. "The movement of neurotransmitter (chemical) 
receptors occurs through little packages that deliver molecules to the synapse 
when new memories form. What we have discovered is the molecular motor that 
moves these packages when synapses are active."

When neurons fire at the same time, their connections strengthen and a person 
can associate certain features. "Once you have heard someone's name, seen his 
face, where he was standing, all these features can be bound into a unified 
packet of information – a percept – and at a very cellular level this occurs by 
strengthening synaptic connections between co-active neurons," said Ehlers, who 
is also a Howard Hughes Medical Investigator.

To learn and make new associations, the brain alters the strengths of the 
synapses' electrical inputs onto cells that compute these features. Scientists 
studied the hippocampus, where memories form, but this machinery could operate 
in other brain areas.

"One of earliest changes in Alzheimer's disease is synapse dysfunction, so this 
molecule might be a new target for that disease," he said. "Abnormal movement 
of receptors may be implicated in brain development, in autism." He said the 
molecule potentially is involved "in the abnormal electrical activity of 
epilepsy and the overactive brain pathways of addiction."

In a series of biochemistry and microscopic imaging experiments, Ehlers and 
colleagues found that the myosin Vb (five-b) molecule in hippocampal neurons 
responded to a flow of calcium ions from the synaptic space by popping up and 
into action. One end of the myosin is attached the meshlike actin filaments so 
it can "walk" to the end of the nerve cells where receptors are. On its other 
end, it tows an endosome, a packet that contains new receptors.

"These endosomes are like little memories waiting to happen," Ehlers said. 
"They are reservoirs of neurotransmitter receptors that brain cells deploy to 
add more receptors to a particular synapse. More receptors equals stronger 
synapses."

Electrical impulses cause one nerve cell to dump its neurotransmitter, in this 
case, glutamate, into the small space between neurons (the synapse), which 
activates neurotransmitter receptors on the receiving side. These are ion 
channels that open in response to neurotransmitter and generate the electrical 
impulse.

When the scientists blocked myosin in single cells, this stopped the addition 
of new receptors and prevented electrical impulses from getting stronger, 
showing that myosin is essential to enhancing nerve cell connections.

"This is a very basic cellular mechanism of brain plasticity. It is likely 
fundamental to brain development and disease," Ehlers said. "The myosin Vb 
molecule gives us a new way to think about designing therapies for treating 
memory loss, psychiatric disease and brain development."

Other authors included Zhiping Wang and Ian G. Davidson of the Duke Department 
of Neurobiology and the Howard Hughes Medical Institute (HHMI); Jeffrey G. 
Edwards, Nathan Riley and Julie A. Kauer of the Department of Molecular 
Pharmacology, Physiology, and Biotechnology at Brown University; D. William 
Provance Jr., Ryan Karcher and John A. Mercer of the McLaughlin Research 
Institute in Great Falls, Montana; and Xiang-dong Li and Mitsuo Ikebe of the 
Department of Physiology, University of Massachusetts Medical School. The work 
was supported by grants from the National Institutes of Health and the HHMI.
Adapted from materials provided by Duke University Medical Center.
Need to cite this story in your essay, paper, or report? Use one of the 
following formats:
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MLA
Duke University Medical Center (2008, November 1). Scientists Identify 
Machinery That Helps Make Memories. ScienceDaily. Retrieved November 2, 2008, 
from http://www.sciencedaily.com­ /releases/2008/10/081030123821.htm


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