ArticleProceedings of the National Academy of Sciences of the United States of America1994
A direct mechanism for sensing low oxygen levels by central neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 116 citations in OpenAlex.
- Acute intermittent hypoxia in neonatal rodent central nervous system facilitates respiratory frequency through the recruitment of hypothalamic areas.Experimental physiology · 2025Article
- Impact of High-Altitude Hypoxia on Bone Defect Repair: A Review of Molecular Mechanisms and Therapeutic Implications.Frontiers in medicine · 2022Review
- Knockdown of a Cyclic Nucleotide-Gated Ion Channel Impairs Locomotor Activity and Recovery From Hypoxia in AdultFrontiers in physiology · 2022Article
- Chronic Intermittent Hypoxia-Induced Aberrant Neural Activities in the Hippocampus of Male Rats Revealed by Long-TermFrontiers in cellular neuroscience · 2021Article
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Modeling the effects of extracellular potassium on bursting properties in pre-Bötzinger complex neurons.Journal of computational neuroscience · 2016Article
- Hypoxemia, oxygen content, and the regulation of cerebral blood flow.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Review
- Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration.Translational stroke research · 2014Review
- Statistical assessment of the stability of neural movement representations.Journal of neurophysiology · 2011Article
- Significance of brain tissue oxygenation and the arachidonic acid cascade in stroke.Antioxidants & redox signaling · 2011Review
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Sensory adaptation and short term plasticity as Bayesian correction for a changing brain.PloS one · 2010Article
- Catecholamine secretion from rat foetal adrenal chromaffin cells and hypoxia sensitivity.Pflugers Archiv : European journal of physiology · 2007Article
- Hypoxia-induced changes in neuronal network properties.Molecular neurobiology · 2005Review
- A preferential role for glycolysis in preventing the anoxic depolarization of rat hippocampal area CA1 pyramidal cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Effect of acute hypoxia on ATP-sensitive potassium currents in substantia gelatinosa neurons of juvenile rats.Pflugers Archiv : European journal of physiology · 2003Article
- Enhanced spontaneous transmitter release is the earliest consequence of neocortical hypoxia that can explain the disruption of normal circuit function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Oxygen-sensing persistent sodium channels in rat hippocampus.The Journal of physiology · 2000Article
- Hypoxic pulmonary vasoconstriction: role of voltage-gated potassium channels.Respiratory research · 2000Review
- Nitric oxide increases persistent sodium current in rat hippocampal neurons.The Journal of physiology · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cascade of cellular events that is triggered by low O2 levels in the central nervous system depends on initial sensing mechanisms that can be crucial in determining the overall cell response, adaptation, or injury. In this report, we demonstrate that the activity of an identified K+ channel is regulated directly by environmental O2. Membrane ionic currents were recorded from neurons of the neocortex and the substantia nigra and studied by using whole-cell or excised membrane patches. O2 deprivation reversibly induced an initial transient increase in whole-cell outward currents, and this was followed by a pronounced decrease in these currents. In cell-free excised membrane patches, lack of O2 reversibly inhibited a class of K+ channels that are inhibited by ATP and activated by Ca2+. K+ channel inhibition depended on pO2 level, with a 50% inhibition at approximately 11 torr (1 torr = 6.9 kPa). By the use of specific agents that chelate metal in metal-containing O2-sensing centers, including heme, nonheme iron, copper, and flavin, we also demonstrated that iron-center but not copper-center blockers inhibited the channel in excised patches in a similar fashion as low pO2. These results strongly suggest that K+ channel activity is modulated during O2 deprivation by nonheme iron-containing proteins that are associated with channel molecules, thus providing evidence for a direct O2-sensing mechanism in neuronal membranes.
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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.