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Article: Triggers and the Opening of Ion Channels

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  • Robert Karl Stonjek
    TRIGGERS AND THE OPENING OF ION CHANNELS The following points are made by Cynthia Czajkowski (Nature 2005 438:167): 1) Chemical signalling in the brain
    Message 1 of 1 , Dec 3, 2005
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      TRIGGERS AND THE OPENING OF ION CHANNELS

      The following points are made by Cynthia Czajkowski (Nature 2005 438:167):

      1) Chemical signalling in the brain involves the rapid opening and closing of channels known as ligand-gated ion channels, which lie in the membranes of nerve cells. Binding of a specific activator (a ligand) to these proteins triggers the opening of an integral pore through the membrane in as little as tens of microseconds. Although we know a fair amount about the structure of ligand-gated ion channels, the mechanisms by which the binding of a ligand triggers channel opening are still under debate. New work identifies a network of interacting amino-acid residues in one such protein, and reveals a pathway by which changes at the protein's ligand-binding site can be propagated to its channel region. Further new work identifies a proline residue that acts as a molecular switch to control channel opening. Together, the two reports provide a compelling description of the structural machinery that couples ligand binding to channel gating.

      2) Communication between nerve cells takes place at junctions called synapses. When a presynaptic cell is activated, it releases neurochemicals (neurotransmitters) across the synapse that bind to ligand-gated ion channels on the surface of the postsynaptic cell. Binding of neurotransmitter causes the channels to open, allowing ions to flood across the postsynaptic-cell membrane and change the cell's activity. So ligand-gated ion channels can be thought of as transducers that rapidly convert chemical signals into an electrical output. Their opening and closing regulate information flow throughout the brain, and mutations in these channels are responsible for a number of "channelopathies", such as congenital myasthenic syndromes, epileptic disorders, and hereditary hyperekplexia.

      Full Text at ScienceWeek
      http://scienceweek.com/2005/sw051209-3.htm

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      Robert Karl Stonjek

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