Abstract:
:Changes in the intracellular Ca2+ concentration ([Ca2+]i) induced by ischemia in vitro (oxygen-glucose deprivation) were continuously recorded using fura-2-loaded hippocampal slices under normal (pH 7.4), acidotic (pH 6.8) and alkalotic (pH 7.8) conditions. Oxygen-glucose deprivation induced an initial slow and a subsequent characteristic rapid increase in [Ca2+]i in most of the normal and alkalotic preparations regardless of whether or not Ca2+ was present in the bathing solutions. This characteristic rapid increase in [Ca2+]i was observed in a minority of the acidotic preparations and its latency was significantly longer in acidotic preparations than in normal and alkalotic preparations. The rise in [Ca2+]i at 10 min of oxygen-glucose deprivation was significantly smaller in the acidotic preparations than in the normal and alkalotic preparations, regardless of whether or not Ca2+ was present. At 15 min, the differences in the increase in [Ca2+]i between normal and acidotic preparations in Ca(2+)-containing solutions (2.5 mM) were insignificant. However, significant differences were still observed between the acidotic preparations and either the normal or alkalotic preparations under Ca(2+)-free conditions. These results suggest that acidosis inhibits the ischemia-induced rise in [Ca2+]i by attenuating both Ca2+ influx from the extracellular space and Ca2+ release from intracellular sites.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Ebine Y,Fujiwara N,Shimoji Kdoi
10.1016/0304-3940(94)90439-1subject
Has Abstractpub_date
1994-02-28 00:00:00pages
155-8issue
1-2eissn
0304-3940issn
1872-7972pii
0304-3940(94)90439-1journal_volume
168pub_type
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