ArticleNeurochemical research2005
Endoplasmic reticulum dysfunction and Ca2+ deregulation in isolated CA1 neurons during oxygen and glucose deprivation.
Article in Neurochemical research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Computer models predict differential dendritic vulnerability with ischemia and spreading depression.PLoS computational biology · 2026Article
- Computer models predict differential dendritic vulnerability with ischemia and spreading depression.bioRxiv : the preprint server for biology · 2025Article
- STING, the Endoplasmic Reticulum, and Mitochondria: Is Three a Crowd or a Conversation?Frontiers in immunology · 2020Review
- Dantrolene enhances the protective effect of hypothermia on cerebral cortex neurons.Neural regeneration research · 2015Article
- Intermittent hypothermia is neuroprotective in an in vitro model of ischemic stroke.International journal of biological sciences · 2014Article
- Painful nerve injury decreases sarco-endoplasmic reticulum Ca²⁺-ATPase activity in axotomized sensory neurons.Neuroscience · 2013Article
- Orais and STIMs: physiological mechanisms and disease.Journal of cellular and molecular medicine · 2012Review
- A novel method for inducing focal ischemia in vitro.Journal of neuroscience methods · 2010Article
- Intracellular- and extracellular-derived Ca(2+) influence phospholipase A(2)-mediated fatty acid release from brain phospholipids.Biochimica et biophysica acta · 2009Review
- Mitochondria are more resistant to hypoxic depolarization in the newborn than in the adult brain.Neurochemical research · 2008Article
- Differential changes in pyridoxine 5'-phosphate oxidase immunoreactivity and protein levels in the somatosensory cortex and striatum of the ischemic gerbil brain.Neurochemical research · 2008Article
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Authors and funding
5 authors.
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Abstract
Intracellular calcium ([Ca2+]i) plays a pivotal role in neuronal ischemia. The aim of the present study was to investigate the routes of Ca2+ entry during non-excitotoxic oxygen and glucose deprivation (OGD) in acutely dissociated rat CA1 neurons. During OGD the fluo-3/fura red ratio reflecting [Ca2+]i increased rapidly and irreversibly. [Ca2+]i increased to the same degree in Ca2 + depleted medium, and also when both the ryanodine receptors (RyR) and the inositol 1,4,5-trisphosphate (IP3) receptors were blocked. When the endoplasmic reticulum (ER) Ca2+ stores were emptied with thapsigargin no increase in [Ca2+]i was observed independent of extracellular Ca2+. The OGD induced Ca2+ deregulation in isolated CA1 neurons is not prevented by removing Ca2+, or by blocking the IP3- or RyR receptors. However, when SERCA was blocked, no increase in [Ca2+]i was observed suggesting that SERCA dysfunction represents an important mechanism for ischemic Ca2+ overload.
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Registered trials
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