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  • Articles: DFG German National Licenses  (2)
  • 2000-2004  (2)
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  • Articles: DFG German National Licenses  (2)
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Years
Year
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 79 (2001), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Microfluorimetric measurements of intracellular calcium ion concentration [Ca2+]i were employed to examine the effects of chronic hypoxia (2.5% O2, 24 h) on Ca2+ stores and capacitative Ca2+ entry in human neuroblastoma (SH-SY5Y) cells. Activation of muscarinic receptors evoked rises in [Ca2+]i which were enhanced in chronically hypoxic cells. Transient rises of [Ca2+]i evoked in Ca2+-free solutions were greater and decayed more slowly following exposure to chronic hypoxia. In control cells, these transient rises of [Ca2+]i were also enhanced and slowed by removal of external Na+, whereas the same manoeuvre did not affect responses in chronically hypoxic cells. Capacitative Ca2+ entry, observed when re-applying Ca2+ following depletion of intracellular stores, was suppressed in chronically hypoxic cells. Western blots revealed that presenilin-1 levels were unaffected by chronic hypoxia. Exposure of cells to amyloid β peptide (1–40) also increased transient [Ca2+]i rises, but did not mimic any other effects of chronic hypoxia. Our results indicate that chronic hypoxia causes increased filling of intracellular Ca2+ stores, suppressed expression or activity of Na+/Ca2+ exchange and reduced capacitative Ca2+ entry. These effects are not attributable to increased amyloid β peptide or presenilin-1 levels, but are likely to be important in adaptive cellular remodelling in response to prolonged hypoxic or ischemic episodes.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Prolonged hypoxia exerts profound effects on cell function, and has been associated with increased production of amyloid β peptides (AβPs) of Alzheimer's disease. Here, we have investigated the effects of chronic hypoxia (2.5% O2, 24 h) on capacitative Ca2+ entry (CCE) in primary cultures of rat type-I cortical astrocytes, and compared results with those obtained in astrocytes exposed to AβPs. Chronic hypoxia caused a marked enhancement of CCE that was observed after intracellular Ca2+ stores were depleted by bradykinin application or by exposure to thapsigargin (1 µm). Exposure of cells for 24 h to 1 µm AβP(1−40) did not alter CCE. Enhancement of CCE was not attributable to cell hyperpolarization, as chronically hypoxic cells were significantly depolarized as compared with controls. Mitochondrial inhibition [by FCCP (10 µm) and oligomycin (2.5 µg/mL)] suppressed CCE in all three cell groups, but more importantly there were no significant differences in the magnitude of CCE in the three astrocyte groups under these conditions. Similarly, the antioxidants melatonin and Trolox abolished the enhancement of CCE in hypoxic cells. Our results indicate that chronic hypoxia augments CCE in cortical type-I astrocytes, a finding which is not mimicked by AβP(1−40) and appears to be dependent on altered mitochondrial function.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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