1996
DOI: 10.1523/jneurosci.16-01-00071.1996
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In vitro ischemia promotes calcium influx and intracellular calcium release in hippocampal astrocytes

Abstract: The intracellular calcium concentration ([Ca2']J of astrocytes within rat hippocampal slices was measured during simultaneous hypoxia and hypoglycemia to examine the early intracellular signaling events induced by this in vitro model of ischemia.

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Cited by 124 publications
(86 citation statements)
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“…Ca 2 þ -stimulated production of ATP was initially characterized in cardiac muscle mitochondria, which increased energy production up to 10-fold faster than stimulation by ADP. 23 Here, we tested and extended 24 However, the functional implications of Ca 2 þ following ischemia have not been resolved, with both protective and detrimental effects identified. Several groups reported that IP 3 -Ca 2 þ signaling counteracted the development of ischemic brain edema via its role in regulatory volume decrease.…”
Section: Discussionmentioning
confidence: 99%
“…Ca 2 þ -stimulated production of ATP was initially characterized in cardiac muscle mitochondria, which increased energy production up to 10-fold faster than stimulation by ADP. 23 Here, we tested and extended 24 However, the functional implications of Ca 2 þ following ischemia have not been resolved, with both protective and detrimental effects identified. Several groups reported that IP 3 -Ca 2 þ signaling counteracted the development of ischemic brain edema via its role in regulatory volume decrease.…”
Section: Discussionmentioning
confidence: 99%
“…In particular, in the presence of Ca 2ϩ channel antagonists, the [C a 2ϩ ] i increase on high K ϩ depolarization in both acutely dissociated astrocytes (Duffy and MacVicar, 1994) and astrocytes from hippocampal slices was observed to be, at least partially, inhibited (Porter and McCarthy, 1995;Duff y and MacVicar, 1996). Although we obtained similar results, our interpretation is that C a 2ϩ VOC antagonists reduce the [C a 2ϩ ] i increase in astrocytes on K ϩ stimulation by blocking neuronal C a 2ϩ channels, thus causing a reduction in neurotransmitter release.…”
Section: Discussionmentioning
confidence: 99%
“…In previous studies on acutely isolated astrocytes (Duffy and MacVicar, 1994) and astrocytes from acute brain slices (Porter and McC arthy, 1995;Duff y and MacVicar, 1996), it has been demonstrated that the C a 2ϩ VOC antagonist verapamil potently inhibits the [C a 2ϩ ] i increase in astrocytes caused by high K ϩ stimulation. This observation was interpreted as an indication for the expression of C a 2ϩ VOC s in astrocytes in situ and for their crucial role in mediating the [C a 2ϩ ] i increase in these cells on K ϩ stimulation.…”
Section: Ca 2؉ Vocs Do Not Contribute To the K ؉ -Induced [Ca 2؉ ] I mentioning
confidence: 97%
“…Synaptic activity induces the activation of various neurotransmitter receptors, which in turn leads to intracellular Ca 2ϩ increases in astrocytes (Porter and McCarthy, 1996;Latour et al, 2001). The extracellular accumulation of K ϩ resulting from neuronal high-frequency stimulation also induces Ca 2ϩ influx in astrocytes through voltage-gated Ca 2ϩ channels (Duffy and MacVicar, 1996;Latour et al, 2001). Astrocyte-induced modulation of synaptic transmission is likely attributable to glutamate released via Ca 2ϩ -and SNARE protein-dependent exocytosis (Araque et al, 2000).…”
Section: Introductionmentioning
confidence: 99%