ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Sodium influx pathways during and after anoxia in rat hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- A dangerous liaison: Spreading depolarization and tissue acidification in cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- Acid-sensing ion channel 1 contributes to pulmonary arterial smooth muscle cell depolarization following hypoxic pulmonary hypertension.The Journal of physiology · 2021Article
- TRPM4 and the Emperor.Channels (Austin, Tex.) · 2018Article
- TRPM4 activation by chemically- and oxygen deprivation-induced ischemia and reperfusion triggers neuronal death.Channels (Austin, Tex.) · 2017Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Excessive Na+/H+ exchange in disruption of dendritic Na+ and Ca2+ homeostasis and mitochondrial dysfunction following in vitro ischemia.The Journal of biological chemistry · 2010Article
- Temporary sequestration of potassium by mitochondria in astrocytes.The Journal of biological chemistry · 2010Article
- Presynaptic glycine receptors influence plasma membrane potential and glutamate release.Neurochemical research · 2010Article
- Non-synaptic receptors and transporters involved in brain functions and targets of drug treatment.British journal of pharmacology · 2010Review
- Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?Progress in neurobiology · 2010Review
- THE ROLE OF INTRACELLULAR SODIUM (Na) IN THE REGULATION OF CALCIUM (Ca)-MEDIATED SIGNALING AND TOXICITY.Health · 2010Article
- The importance of systemic response in the pathobiology of blast-induced neurotrauma.Frontiers in neurology · 2010Article
- Regulation of early neurite morphogenesis by the Na+/H+ exchanger NHE1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Na,K-ATPase activity regulates AMPA receptor turnover through proteasome-mediated proteolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Activation of DOR attenuates anoxic K+ derangement via inhibition of Na+ entry in mouse cortex.Cerebral cortex (New York, N.Y. : 1991) · 2008Article
- The Role of Intracellular Sodium in the Regulation of NMDA-Receptor-Mediated Channel Activity and Toxicity.Molecular neurobiology · 2006Review
- Decreased neuronal death in Na+/H+ exchanger isoform 1-null mice after in vitro and in vivo ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanisms that contribute to Na+ influx during and immediately after 5 min anoxia were investigated in cultured rat hippocampal neurons loaded with the Na+-sensitive fluorophore sodium-binding benzofuran isophthalate. During anoxia, an influx of Na+ in the face of reduced Na+,K+-ATPase activity caused a rise in [Na+]i. After the return to normoxia, Na+,K+-ATPase activity mediated the recovery of [Na+]i despite continued Na+ entry. Sodium influx during and after anoxia occurred through multiple pathways and increased the longer neurons were maintained in culture. Under the experimental conditions used, Na+ entry during anoxia did not reflect the activation of ionotropic glutamate receptors, TTX- or lidocaine-sensitive Na+ channels, plasmalemmal Na+/Ca2+ exchange, Na+/H+ exchange, or HCO3--dependent mechanisms; rather, contributions were received from a Gd3+-sensitive pathway activated by reactive oxygen species and Na+/K+/2Cl- cotransport in neurons maintained for 6-10 and 11-14 d in vitro (DIV), respectively. Sodium entry immediately after anoxia was not attributable to the activation of ionotropic glutamate receptors, voltage-activated Na+ channels, or Na+/K+/2Cl- cotransport; rather, it occurred via Na+/Ca2+ exchange, Na+/H+ exchange, and a Gd3+-sensitive pathway similar to that observed during anoxia; 11-14 DIV neurons received an additional contribution from an -dependent mechanism(s). The results provide insight into the intrinsic mechanisms that contribute to disturbed internal Na+ homeostasis during and immediately after anoxia in rat hippocampal neurons and, in this way, may play a role in the pathogenesis of anoxic or ischemic cell injury.
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