A model for exocytosis based on the opening of calcium-activated potassium channels in vesicles.
It is proposed that the role of calcium in calcium-induced exocytosis is to open Ca-activated K channels present in vesicle membranes. The opening of these channels coupled with anion transport across the vesicle membranes would result in an influx of K and anions, increasing the osmotic pressure of the vesicles. For those vesicles situated very close to the cell plasma membrane, this would lead to fusion with the membrane and exocytosis of the vesicle contents. This model can account for facilitation and other key properties of transmitter release. In addition, the model predicts that vesicles with a higher transmitter content, and hence higher initial osmotic pressure, would be preferentially discharged. The model also predicts that a faster response can be obtained for small vesicles than for large vesicles, providing a rationale as to why neurotransmitters, which must be released quickly, are packaged in small vesicles.
Stanley
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EF
Ehrenstein
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D000200:Action Potentials; D002118:Calcium / Q000494:pharmacology*; D002462:Cell Membrane / Q000502:physiology*; D002463:Cell Membrane Permeability; D003593:Cytoplasm / Q000378:metabolism; D005089:Exocytosis / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials; D008954:Models, Biological; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*
D007473:Ion Channels; D011188:Potassium; D002118:Calcium