• Medientyp: E-Artikel
  • Titel: The Na+‐Ca2+ exchange system in rat glial cells in culture: Activation by external monovalent cations
  • Beteiligte: Holgado, Andrea; Beaugé, Luis
  • Erschienen: Wiley, 1995
  • Erschienen in: Glia
  • Sprache: Englisch
  • DOI: 10.1002/glia.440140202
  • ISSN: 0894-1491; 1098-1136
  • Schlagwörter: Cellular and Molecular Neuroscience ; Neurology
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  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>Cultured rat glial cells display a Na<jats:sup>+</jats:sup>‐Ca<jats:sup>2+</jats:sup> exchange system located at the plasma membrane levels. This was evidenced by the Na<jats:sup>+</jats:sup> (i)‐dependency of a Na<jats:sup>+</jats:sup> (o)‐inhibitable influx of Ca<jats:sup>2+</jats:sup>, or reversal exchange mode. This antiporter has an external site where monovalent cations (K<jats:sup>+</jats:sup>, Li<jats:sup>+</jats:sup>, and Na<jats:sup>+</jats:sup> were investigated) stimulate the exchange by a chemical action. The monovalent cation is not transported during the exchange cycle. The mechanism of that stimulation agrees with an increase in the apparent affinity of the carrier for Ca<jats:sup>2+</jats:sup> (o) without effect on the maximal translocation rate. Two models can equally well account for the data: i) the formation of ECa(o) is essential for the binding of the monovalent cation, or ii) the activating cation can bind even when the carrier is free of Ca<jats:sup>2+</jats:sup>(o). The cations K<jats:sup>+</jats:sup> and Li<jats:sup>+</jats:sup> produced only stimulation, although that of K<jats:sup>+</jats:sup> seem to require actions other than the chemical effect. The response to Na<jats:sup>+</jats:sup> was biphasic; this can be fully explained considering that at low concentrations, Na<jats:sup>+</jats:sup>(o) binds preferentially to the activating monovalent site while at high concentrations it displaces Ca<jats:sup>2+</jats:sup> from its external transporting site. Pure type I astrocytes displayed the same Na<jats:sup>+</jats:sup>‐Ca<jats:sup>2+</jats:sup> exchange mechanism. © 1995 Wiley‐Liss, Inc.</jats:p>