ArticleBrain : a journal of neurology2010
The role of pannexin hemichannels in the anoxic depolarization of hippocampal pyramidal cells.
Article in Brain : a journal of neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Spreading depolarization: A wave that precedes and drives cerebral ischemic cell death-Target for neuroprotection.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Mechanistic insight into the initiation of spreading depolarizations: Is it really all about potassium?The Journal of physiology · 2025Article
- How to Pick a Neuroprotective Drug in Stroke Without Losing Your Mind?Life (Basel, Switzerland) · 2025Review
- Advancements in Targeting Ion Channels for the Treatment of Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- NMDAR-mediated activation of pannexin1 channels contributes to the detonator properties of hippocampal mossy fiber synapses.iScience · 2024Article
- Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization.Neurocritical care · 2022Article
- The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention.Neurocritical care · 2022Review
- Altered neocortical oscillations and cellular excitability in an in vitro Wwox knockout mouse model of epileptic encephalopathy.Neurobiology of disease · 2021Article
- The role of spreading depolarizations and electrographic seizures in early injury progression of the rat photothrombosis stroke model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Review
- Lasting s-ketamine block of spreading depolarizations in subarachnoid hemorrhage: a retrospective cohort study.Critical care (London, England) · 2019Article
- Dynamic Gain Analysis Reveals Encoding Deficiencies in Cortical Neurons That Recover from Hypoxia-Induced Spreading Depolarizations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Adenosine AJournal of neurophysiology · 2019Article
- The negative ultraslow potential, electrophysiological correlate of infarction in the human cortex.Brain : a journal of neurology · 2018Article
- Pannexin-1 is involved in neuronal apoptosis and degeneration in experimental intracerebral hemorrhage in rats.Molecular medicine reports · 2018Article
- Glia and hemichannels: key mediators of perinatal encephalopathy.Neural regeneration research · 2018Review
- Neuronal pannexin-1 channels are not molecular routes of water influx during spreading depolarization-induced dendritic beading.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Functional implications of axon initial segment cytoskeletal disruption in stroke.Acta pharmacologica Sinica · 2016Review
- Pannexin channels and ischaemia.The Journal of physiology · 2015Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal gap junctional hemichannels, composed of pannexin-1 subunits, have been suggested to play a crucial role in epilepsy and brain ischaemia. After a few minutes of anoxia or ischaemia, neurons in brain slices show a rapid depolarization to ∼-20 mV, called the anoxic depolarization. Glutamate receptor blockers can prevent the anoxic depolarization, suggesting that it is produced by a cation influx through glutamate-gated channels. However, in isolated hippocampal pyramidal cells, simulated ischaemia evokes a large inward current and an increase in permeability to large molecules, mediated by the opening of pannexin-1 hemichannels. N-methyl-d-aspartate is also reported to open these hemichannels, suggesting that the activation of N-methyl-d-aspartate receptors, which occurs when glutamate is released in ischaemia, might cause the anoxic depolarization by evoking a secondary ion flux through pannexin-1 hemichannels. We tested the contribution of pannexin hemichannels to the anoxic depolarization in CA1 pyramidal cells in the more physiological environment of hippocampal slices. Three independent inhibitors of hemichannels-carbenoxolone, lanthanum and mefloquine-had no significant effect on the current generating the anoxic depolarization, while a cocktail of glutamate and gamma-aminobutyric acid class A receptor blockers abolished it. We conclude that pannexin hemichannels do not generate the large inward current that underlies the anoxic depolarization. Glutamate receptor channels remain the main candidate for generating the large inward current that produces the anoxic depolarization.
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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.