Metabolic Regulation of Ion Channels
During the last 30 years a great deal of progress has been made in our understanding of how neurotransmitters can regulate the activity of excitable cells. Much of our knowledge has come from studies on the vertebrate neuromuscular junction, in part because the preparation is easily accessible for experimental manipulation, but perhaps more importantly because a series of brilliant investigators have made it the focus of their highly imaginative studies. The resulting body of work has given us a detailed molecular picture of the nicotinic acetylcholine receptor/channel as a single macromolecular complex that can both bind acetylcholine and mediate the transport of ions across the plasma membrane. The opening of the channel (and transport of ions) is rapid in onset after the binding of acetylcholine to the receptor and is rapidly reversible when the receptor is no longer occupied by the agonist. Figure 1A summarizes schematically this way of thinking of rapidly reversible changes in the activity of an ion channel as being dependent on the continued occupation of a closely associated receptor by an agonist.
KeywordsBehavioral Sensitization Protein Kinase Inhibitor Dependent Protein Kinase Excitable Cell Rectify Potassium Channel
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