ArticlePloS one2010
Neuronal Ca2+-activated K+ channels limit brain infarction and promote survival.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- Moderate Ethanol-Preconditioning Offers Ischemic Tolerance Against Focal Cerebral Ischemic/Reperfusion: Role of Large Conductance Calcium-Activated Potassium Channel.Neurochemical research · 2022Article
- The modulation of potassium channels by estrogens facilitates neuroprotection.Frontiers in cell and developmental biology · 2022Review
- Acupuncture ameliorates neurological function in rats with cerebral ischemia-reperfusion by regulating the opening of large-conductance CaBrain and behavior · 2021Article
- BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke.Frontiers in cellular neuroscience · 2021Article
- Oligodendrocytes, BK channels and the preservation of myelin.F1000Research · 2021Review
- The Large-Conductance, Calcium-Activated Potassium Channel: A Big Key Regulator of Cell Physiology.Frontiers in physiology · 2021Review
- Genetic factors for susceptibility to and manifestations of neuromyelitis optica.Annals of clinical and translational neurology · 2020Article
- The salvageable brain in acute ischemic stroke. The concept of a reverse mismatch: a mini-review.Metabolic brain disease · 2020Review
- The Role of Astrocytes in the Central Nervous System Focused on BK Channel and Heme Oxygenase Metabolites: A Review.Antioxidants (Basel, Switzerland) · 2019Review
- Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018Review
- Expression and Activation of BKFrontiers in cardiovascular medicine · 2018Article
- Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, CaNeuroscience bulletin · 2017Article
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Decreased calcium-activated potassium channels by hypoxia causes abnormal firing in the spontaneous firing medial vestibular nuclei neurons.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2015Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- The large conductance calcium-activated potassium channel affects extrinsic and intrinsic mechanisms of apoptosis.Journal of neuroscience research · 2015Article
- Gene expression profiles of patients with cerebral hematoma following spontaneous intracerebral hemorrhage.Molecular medicine reports · 2014Article
- Critical role of large-conductance calcium- and voltage-activated potassium channels in leptin-induced neuroprotection of N-methyl-d-aspartate-exposed cortical neurons.Pharmacological research · 2014Article
- The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis.BMC genomics · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal calcium-activated potassium channels of the BK type are activated by membrane depolarization and intracellular Ca(2+) ions. It has been suggested that these channels may play a key neuroprotective role during and after brain ischemia, but this hypothesis has so far not been tested by selective BK-channel manipulations in vivo. To elucidate the in vivo contribution of neuronal BK channels in acute focal cerebral ischemia, we performed middle cerebral artery occlusion (MCAO) in mice lacking BK channels (homozygous mice lacking the BK channel alpha subunit, BK(-/-)). MCAO was performed in BK(-/-) and WT mice for 90 minutes followed by a 7-hour-reperfusion period. Coronal 1 mm thick sections were stained with 2,3,5-triphenyltetrazolium chloride to reveal the infarction area. We found that transient focal cerebral ischemia by MCAO produced larger infarct volume, more severe neurological deficits, and higher post-ischemic mortality in BK(-/-) mice compared to WT littermates. However, the regional cerebral blood flow was not significantly different between genotypes as measured by Laser Doppler (LD) flowmetry pre-ischemically, intra-ischemically, and post-ischemically, suggesting that the different impact of MCAO in BK(-/-) vs. WT was not due to vascular BK channels. Furthermore, when NMDA was injected intracerebrally in non-ischemic mice, NMDA-induced neurotoxicity was found to be larger in BK(-/-) mice compared to WT. Whole-cell patch clamp recordings from CA1 pyramidal cells in organotypic hippocampal slice cultures revealed that BK channels contribute to rapid action potential repolarization, as previously found in acute slices. When these cultures were exposed to ischemia-like conditions this induced significantly more neuronal death in BK(-/-) than in WT cultures. These results indicate that neuronal BK channels are important for protection against ischemic brain damage.
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Registered trials
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