ArticleNeurochemical research2007
Changes in the spontaneous calcium oscillations for the development of the preconditioning-induced ischemic tolerance in neuron/astrocyte co-culture.
Article in Neurochemical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- Massive efflux of adenosine triphosphate into the extracellular space immediately after experimental traumatic brain injury.Experimental and therapeutic medicine · 2021Article
- PACAP modulation of calcium ion activity in developing granule cells of the neonatal mouse olfactory bulb.Journal of neurophysiology · 2015Article
- Transient cerebral ischemia induces active astrocytosis without distinct neuronal death in the gerbil main olfactory bulb: a long-term analysis.Neurochemical research · 2010Article
- Simulation of spontaneous Ca2+ oscillations in astrocytes mediated by voltage-gated calcium channels.Biophysical journal · 2009Article
- Possible involvement of extracellular ATP-P2Y purinoceptor signaling in ischemia-induced tolerance of astrocytes in culture.Neurochemical research · 2009Article
- Elevated synaptic activity preconditions neurons against an in vitro model of ischemia.The Journal of biological chemistry · 2008Article
- Nitric oxide-mediated modulation of synaptic activity by astrocytic P2Y receptors.The Journal of general physiology · 2008Article
- Therapeutic Potential of Astrocyte Transplantation.Cell transplantationReview
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5 authors at 1 institution in 1 country.
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Abstract
Spontaneous Ca(2+) oscillations are believed to contribute to the regulation of gene expression. Here we investigated whether and how the dynamics of Ca(2+) oscillations changed after sublethal preconditioning (PC) for PC-induced ischemic tolerance in neuron/astrocyte co-cultures. The frequency of spontaneous Ca(2+) oscillations significantly decreased between 4 and 8 h after the end of PC in both neurons and astrocytes. Treatment with 2-APB, an inhibitor of IP3 receptors, decreased the oscillatory frequency, induced ischemic tolerance and a down-regulation of glutamate transporter GLT-1 contributing to the increase in the extracellular glutamate during ischemia. The expression of GLT-1 is known to be up-regulated by PACAP. Treatment with PACAP38 increased the oscillatory frequency, and antagonized both the PC-induced down-regulation of GLT-1 and ischemic tolerance. These results suggested that the PC suppressed the spontaneous Ca(2+) oscillations regulating the gene expressions of various proteins, especially of astrocytic GLT-1, for the development of the PC-induced ischemic tolerance.
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