ArticleThe Journal of physiology2000
Oxygen-sensing persistent sodium channels in rat hippocampus.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 73 citations in OpenAlex.
- Acute intermittent hypoxia in neonatal rodent central nervous system facilitates respiratory frequency through the recruitment of hypothalamic areas.Experimental physiology · 2025Article
- Pathophysiology of ion channels in amyotrophic lateral sclerosis.Molecular brain · 2023Review
- Intracellular activation of full-length human TREK-1 channel by hypoxia, high lactate, and low pH denotes polymodal integration by ischemic factors.Pflugers Archiv : European journal of physiology · 2021Article
- SUMOylation of NaeLife · 2016Article
- Ionic mechanisms maintaining action potential conduction velocity at high firing frequencies in an unmyelinated axon.Physiological reports · 2016Article
- Modeling the effects of extracellular potassium on bursting properties in pre-Bötzinger complex neurons.Journal of computational neuroscience · 2016Article
- Systemic Radical Scavenger Treatment of a Mouse Model of Rett Syndrome: Merits and Limitations of the Vitamin E Derivative Trolox.Frontiers in cellular neuroscience · 2016Article
- Protracted brain development in a rodent model of extreme longevity.Scientific reports · 2015Article
- The free radical scavenger Trolox dampens neuronal hyperexcitability, reinstates synaptic plasticity, and improves hypoxia tolerance in a mouse model of Rett syndrome.Frontiers in cellular neuroscience · 2014Article
- Astrocytes expressing mutant SOD1 and TDP43 trigger motoneuron death that is mediated via sodium channels and nitroxidative stress.Frontiers in cellular neuroscience · 2014Article
- Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability.Journal of neurophysiology · 2013Article
- Voltage-gated Na(+) channels in chemoreceptor afferent neurons--potential roles and changes with development.Respiratory physiology & neurobiology · 2013Review
- Early pathogenesis in the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.Journal of cellular biochemistry · 2012Article
- Modulation of K(ATP) currents in rat ventricular myocytes by hypoxia and a redox reaction.Acta pharmacologica Sinica · 2009Article
- H(2)O(2)-mediated modulation of cytosolic signaling and organelle function in rat hippocampus.Pflugers Archiv : European journal of physiology · 2009Article
- Heme oxygenase is necessary for the excitatory response of cultured neonatal rat rostral ventrolateral medulla neurons to hypoxia.American journal of physiology. Regulatory, integrative and comparative physiology · 2009Article
- Redox reaction modulates transient and persistent sodium current during hypoxia in guinea pig ventricular myocytes.Pflugers Archiv : European journal of physiology · 2007Article
- Seizure-like afterdischarges simulated in a model neuron.Journal of computational neuroscience · 2007Article
- Orthodromic spike generation from electrical stimuli in the rat carotid body: implications for the afferent spike generation process.The Journal of physiology · 2007Article
- Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones.Molecular pain · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Persistent sodium channel activity was recorded before and during hypoxia from cell-attached and inside-out patches obtained from cultured hippocampal neurons at a pipette potential (Vp) of +30 mV. Average mean current (IU) of these channels was very low under normoxic conditions and was similar in cell-attached and excised inside-out patches (-0.018 +/- 0.010 and -0.025 +/- 0.008 pA, respectively, n = 24). 2. Hypoxia increased the activity of persistent sodium channels in 10 cell-attached patches (IU increased from -0. 026 +/- 0.016 pA in control to -0.156 +/- 0.034 pA during hypoxia, n = 4, P = 0.013). The increased persistent sodium channel activity was most prominent at a VP between +70 and +30 mV (membrane potential, Vm = -70 to -30 mV) and could be blocked by lidocaine, TTX or R56865 (n = 5). Sodium cyanide (NaCN, 5 mM; 0.5-5 min) increased persistent sodium channel activity in cell-attached patches (n = 3) in a similar manner. 3. Hypoxia also increased sodium channel activity in inside-out patches from hippocampal neurons. Within 2-4 min of exposure to hypoxia, I had increased 9-fold to -0. 18 +/- 0.04 pA (n = 21, P = 0.001). Sodium channel activity increased further with longer exposures to hypoxia. 4. The hypoxia-induced sodium channel activity in inside-out patches could be inhibited by exposure to 10-100 microM lidocaine applied via the bath solution (I = -0.03 +/- 0.01 pA, n = 8) or by perfusion of the pipette tip with 1 microM TTX (I = -0.01 +/- 0.01 pA, n = 3). 5. The reducing agent dithiothreitol (DTT, 2-5 mM) rapidly abolished the increase in sodium channel activity caused by hypoxia in excised patches (I = -0.01 +/- 0.01 pA, n = 4). Similarly, reduced glutathione (GSH, 5-20 mM) also reversed the hypoxia-induced increase in sodium channel activity (IU = -0.02 +/- 0.02 pA, n = 5). 6. These results suggest that persistent sodium channels in neurons can sense O2 levels in excised patches of plasma membrane. Hypoxia triggers an increase in sodium channel activity. The redox reaction involved in increasing the sodium channel activity probably occurs in an auxiliary regulatory protein, co-localized in the plasma membrane.
Indexed as
Identifiers
What OpenQuestion holds
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.