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  • 1
    ISSN: 1573-6903
    Keywords: Ion fluxes ; growth factor ; astrocytes ; rat ; primary cultures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Astroglial cell cultures were derived from newborn rat forebrain and cultured for 5 days in serum containing-, and for an additional 4 days in a serum-free, defined medium. At the end of this 9-day-long period, basic astroglial growth factor (AGF2) was administered to the culture medium (10 ng per ml). Cells were subsequently cultured in AGF2 containing serum-free, defined medium for further two weeks. At definite intervals of culturing, unidirectional influx of both Na+ and K+ (INa and IK, respectively) was determined by applying22Na and42K. The AGF2-treated cultures showed highly increased, amiloride-sensitive INa at the early exposure period (2–8 hours), similar to that we have reported about cultured astroglia exposed to AGF2 for minutes. They also exhibited significant furosemide-sensitive-, while relatively poor ouabain-sensitive component of INa. However, at later periods of exposure to AGF2, INa was significantly reduced, particularly due to the decrease of its amiloride-sensitive component, while its furosemide-sensitive component further increased with the time of AGF2 treatment. In contrast to INa, the IK in the cultures exposed to AGF2 increased significantly in the course of the long-term exposure period, particularly the ouabain-, and furosemide-sensitive-components, while its amiloride-sensitive component, similarly to that of INa, decreased. Our findings show that the initial activation of the Na+/H+ (or K+/H+) exchange, what characterized the cation transport changes by short-term exposure of astroglial cells to AGF2 in our previous study, comes relatively soon to a cessation but activation of the Na+, K+-pump and the furosemide-sensitive Na+ and K+ influxes further increases. Thus, they suggest the possibility that furosemide-sensitive cation movements play a role, besides the Na+, K+-pump, in the control of glial cell differentiation.
    Type of Medium: Electronic Resource
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