ArticleNeuroscience2009
Inositol 1,4,5-triphosphate receptors and NAD(P)H mediate Ca2+ signaling required for hypoxic preconditioning of hippocampal neurons.
Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Autofluorescence and deep learning in early disease detection: biological foundations, clinical applications, and future directions.Frontiers in artificial intelligence · 2026Review
- The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
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- Non-linear actions of physiological agents: Finite disarrangements elicit fitness benefits.Redox biology · 2017Review
- Short-Term Differentiation of Glioblastoma Stem Cells Induces Hypoxia Tolerance.Neurochemical research · 2016Article
- Analysis of weighted co-regulatory networks in maize provides insights into new genes and regulatory mechanisms related to inositol phosphate metabolism.BMC genomics · 2016Article
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- Hypobaric Preconditioning Modifies Group I mGluRs Signaling in Brain Cortex.Neurochemical research · 2015Article
- Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke.Experimental neurology · 2015Review
- Electroacupuncture at different frequencies (5Hz and 25Hz) ameliorates cerebral ischemia-reperfusion injury in rats: possible involvement of p38 MAPK-mediated anti-apoptotic signaling pathways.BMC complementary and alternative medicine · 2015Article
- Malate-Aspartate Shuttle Inhibitor Aminooxyacetate Acid Induces Apoptosis and Impairs Energy Metabolism of Both Resting Microglia and LPS-Activated Microglia.Neurochemical research · 2015Article
- Preconditioning provides neuroprotection in models of CNS disease: paradigms and clinical significance.Progress in neurobiology · 2014Review
- Article
- Malate-aspartate shuttle mediates the intracellular ATP levels, antioxidation capacity and survival of differentiated PC12 cells.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Multifunctional roles of NAD⁺ and NADH in astrocytes.Neurochemical research · 2012Review
- Article
- Metabotropic actions of the volatile anaesthetic sevoflurane increase protein kinase M synthesis and induce immediate preconditioning protection of rat hippocampal slices.The Journal of physiology · 2012Article
- Article
- The potential dual effects of anesthetic isoflurane on Aβ-induced apoptosis.Current Alzheimer research · 2011Article
- Endoplasmic reticulum Ca(2+) handling in excitable cells in health and disease.Pharmacological reviews · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure of neurons to a non-lethal hypoxic stress greatly reduces cell death during subsequent severe ischemia (hypoxic preconditioning, HPC). In organotypic cultures of rat hippocampus, we demonstrate that HPC requires inositol triphosphate (IP3) receptor-dependent Ca2+ release from the endoplasmic reticulum (ER) triggered by increased cytosolic NAD(P)H. Ca2+ chelation with intracellular BAPTA, ER Ca2+ store depletion with thapsigargin, IP3 receptor block with xestospongin, and RNA interference against subtype 1 of the IP3 receptor all blunted the moderate increases in [Ca2+](i) (50-100 nM) required for tolerance induction. Increases in [Ca2+](i) during HPC and neuroprotection following HPC were not prevented with NMDA receptor block or by removing Ca2+ from the bathing medium. Increased NAD(P)H fluorescence in CA1 neurons during hypoxia and demonstration that NADH manipulation increases [Ca2+](i) in an IP3R-dependent manner revealed a primary role of cellular redox state in liberation of Ca2+ from the ER. Blockade of IP3Rs and intracellular Ca2+ chelation prevented phosphorylation of known HPC signaling targets, including MAPK p42/44 (ERK), protein kinase B (Akt) and CREB. We conclude that the endoplasmic reticulum, acting via redox/NADH-dependent intracellular Ca2+ store release, is an important mediator of the neuroprotective response to hypoxic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.