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  • 2000-2004  (1)
  • 1965-1969
  • 1900-1904
  • Capacitance measurements Endogenous ion channels Maitotoxin Nonselective cation channel Stretch-activated cation channel Xenopus laevis oocyte  (1)
Materialart
Erscheinungszeitraum
  • 2000-2004  (1)
  • 1965-1969
  • 1900-1904
Jahr
  • 1
    ISSN: 1432-2013
    Schlagwort(e): Capacitance measurements Endogenous ion channels Maitotoxin Nonselective cation channel Stretch-activated cation channel Xenopus laevis oocyte
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract. The activation of cation channels in oocytes of Xenopus laevis by the marine poison maitotoxin (MTX) was monitored as membrane current (I m), conductance (G m) and membrane surface area determined by continuous measurements of membrane capacitance (C m). When MTX (25 pM) was added to the bathing solution there was an abrupt, large increase in inward membrane currents. Current/voltage relationships (I/V curves) were linear and suggested activation of voltage-independent nonselective cation channels (NSCC). MTX-induced Ca2+-sensitive currents were mainly carried by Na+ and were suppressed by low (0 mM) or high (40 mM) external Ca2+ concentrations and removal of Na+. Gadolinium (Gd3+, 10–500 µM) also had inhibitory effects, demonstrating the possible involvement of stretch-activated cation channels (SACC). In a high concentration (500 µM), amiloride substantially reduced the MTX-activated current while lower amiloride concentrations (50–100 µM) stimulated the current further. Continuous measurements of C m revealed that MTX induced exocytotic delivery and functional insertion of new channel proteins into the plasma membrane, indicated by a Ca2+-dependent increase in membrane surface area by around 28%. From these data we conclude that MTX activates NSCC that require relatively high concentrations of amiloride to be blocked. Furthermore, MTX possibly stimulates activation of Gd3+- and Ca2+-sensitive mechanosensitive cation channels. Stimulation of these channels is achieved by exocytotic delivery and functional insertion of new channels into the plasma membrane in a pathway that depends on the presence of extracellular Ca2+.
    Materialart: Digitale Medien
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