| Posted: July 30, 2009 |
The mystery of how neurons transmit information has been solved |
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(Nanowerk News) The mystery of how neurons transmit information has been solved. EU-funded researchers from Belgium and the US say that while recycling is a major component in the transmission of nerve signals, it is the protein Tweek that is the key player. The findings are published in the journal Neuron.
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Over the years, researchers have identified a number of proteins active in cellular processes, such as vesicle recycling, through innovative genetic screens and biological screening approaches. But this latest study, funded in part by an EU Marie Curie Excellence Grant, has succeeded in shedding new light on a complex issue.
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Nerve signals are transmitted from one nerve cell to another at structures called synapses which are found at the tip of the neuron. Here, synaptic vesicles, which are like small bubbles, transport chemicals called neurotransmitters to the synapse. The vesicles then fuse to the cell's membrane; this process is called exocytosis.
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The nerve cells then take hold of the extra bit of membrane and bring it back into the cell (a process known as endocytosis) so that it can be recycled.
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So what kicks-starts synaptic vesicle recycling? The Tweek protein does. Named after the South Park cartoon character Tweek Tweak, a hyperactive and anxious boy that drinks too much coffee, the protein has been identified and characterised.
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'Tweek is required to maintain normal synaptic vesicle recycling and affects PI [phosphoinositide lipids] availability,' the authors write. 'Our data suggest that Tweek may regulate synaptic vesicle recycling, at least in part, by affecting PI (4,5)P2 [phosphatidylinositol 4,5-bisphosphate] levels or availability at the synapse.'
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According to Hugo Bellen, a Professor of Molecular and Human Genetics at Baylor College of Medicine (BCM) in the US and senior author of the paper, fruit flies lacking Tweek shake in a hyperactive manner. 'Loss of this protein causes endocytic defects', he says.
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The researchers discovered that cells missing Tweek also had low levels of PI(4,5)P2, which is concentrated in the plasma membrane of most cells. Manipulation of the cell's activity to boost PI(4,5)P2 levels helped suppress the defect in endocytosis of the vesicles.
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The team carried out genetic screens to identify proteins that affect synaptic transmission and plasticity in flies carrying random chemically induced mutations.
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The study revealed that by supplying the Tweek protein to mutant neurons lacking the gene, the endocytic defects are reversed. According to the researchers, most species have Tweek but it is difficult to locate as it occurs in very tiny quantities in the cell.
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'We concluded that the protein Tweek plays a role in making sure the right amounts of PI(4,5)P2 are there so that other proteins can be recruited to the endocytic zone,' Professor Bellen said.
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Also participating in the study were researchers from the Belgium-based Flanders Institute for Biotechnology (VIB) and Katholieke Universiteit Leuven (K.U. Leuven), and the Yale University School of Medicine in the US.
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