ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Enhanced spontaneous transmitter release is the earliest consequence of neocortical hypoxia that can explain the disruption of normal circuit function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 118 citations in OpenAlex.
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- Ischemic Stroke: Pathophysiology and Evolving Treatment Approaches.Neuroscience insights · 2024Review
- In the fast lane: Receptor trafficking during status epilepticus.Epilepsia open · 2023Review
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- The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention.Neurocritical care · 2022Review
- Migraine Aura, Transient Ischemic Attacks, Stroke, and Dying of the Brain Share the Same Key Pathophysiological Process in Neurons Driven by Gibbs-Donnan Forces, Namely Spreading Depolarization.Frontiers in cellular neuroscience · 2022Review
- Headache in people with epilepsy.Nature reviews. Neurology · 2021Review
- Neuregulin-1 inhibits CoClMolecular brain · 2020Article
- Flavin Adenine Dinucleotide Fluorescence as an Early Marker of Mitochondrial Impairment During Brain Hypoxia.International journal of molecular sciences · 2020Article
- The Neurology of Death and the Dying Brain: A Pictorial Essay.Frontiers in neurology · 2020Review
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- Rapid Changes in Synaptic Strength After Mild Traumatic Brain Injury.Frontiers in cellular neuroscience · 2019Article
- Dissipation of transmembrane potassium gradient is the main cause of cerebral ischemia-induced depolarization in astrocytes and neurons.Experimental neurology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After the onset of an acute episode of arrested circulation to the brain and consequent cerebral hypoxia, EEG changes and modifications of consciousness ensue within seconds. This in part reflects the rapid effect of hypoxia on the neocortex, where oxygen deprivation leads to impaired neuronal excitability and abnormal synaptic transmission. To identify the cellular mechanisms responsible for the earliest changes in neocortical function and to determine their time course, we have used patch-in-slice recording techniques to investigate the effects of acute hypoxia on the synaptic and intrinsic properties of layer 5 neurons. Coronal slices of mouse somatosensory cortex were maintained at 37 degrees C and challenged with episodes of hypoxia (3-4 min of exposure to 95% N(2), 5% CO(2)). In recordings with cell-attached patch electrodes, activation of ATP-sensitive potassium channels first became detectable 211 +/- 11 sec (range, 185-240 sec; n = 6 patches) after the onset of hypoxia. Similar recording techniques revealed no alterations in the properties of Na(+) currents in the first 4 min after the onset of hypoxia. The earliest hypoxia-induced disturbance was a marked increase in the frequency of spontaneous EPSCs and IPSCs, which began within 15-30 sec of the removal of oxygen. This rapid synaptic effect was not sensitive to TTX and was present in Ca(2+)-free perfusate, indicating that the hypoxia had a direct influence on the vesicular release mechanisms. The incoherent, massive increase in miniature PSCs would be expected to deplete the readily releasable pool of vesicles in cortical terminals, and to thereby markedly distort the neuronal interactions that underlie normal circuit function.
Indexed as
Identifiers
11425888PMC6762367W1585200182What 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.