ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011
Activation of the central histaminergic system is involved in hypoxia-induced stroke tolerance in adult mice.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- Dose of remote limb ischemic conditioning for enhancing learning in healthy young adults.Experimental brain research · 2019Trial
- A quest for a histaminergic or orexinergic biomarker for sudden infant death syndrome.Pediatric research · 2026Article
- Histamine in the Crosstalk Between Innate Immune Cells and Neurons: Relevance for Brain Homeostasis and Disease.Current topics in behavioral neurosciences · 2022Review
- Anti-Inflammatory Dipeptide, a Metabolite from Ambioba Secretion, Protects Cerebral Ischemia Injury by Blocking Apoptosis Via p-JNK/Bax Pathway.Frontiers in pharmacology · 2021Article
- Ligustilide Attenuates Ischemia Reperfusion-Induced Hippocampal Neuronal ApoptosisFrontiers in pharmacology · 2020Article
- Urolithin A-activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo.CNS neuroscience & therapeutics · 2019Article
- Somatic autophagy of axonal mitochondria in ischemic neurons.The Journal of cell biology · 2019Article
- Is there a central role for the cerebral endothelium and the vasculature in the brain response to conditioning stimuli?Conditioning medicine · 2018Article
- Complement Component C3 Promotes Cerebral Ischemia/Reperfusion Injury Mediated by TLR2/NFκB Activation in Diabetic Mice.Neurochemical research · 2018Article
- Increased risk of brain cancer incidence in stroke patients: a clinical case series, population-based and longitudinal follow-up study.Oncotarget · 2017Article
- BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2.Autophagy · 2017Article
- ADAMTS13 controls vascular remodeling by modifying VWF reactivity during stroke recovery.Blood · 2017Article
- PARK2-dependent mitophagy induced by acidic postconditioning protects against focal cerebral ischemia and extends the reperfusion window.Autophagy · 2017Article
- Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, CaNeuroscience bulletin · 2017Article
- Neuroprotective potential of exercise preconditioning in stroke.Conditioning medicine · 2017Article
- Heterogeneity of B Cell Functions in Stroke-Related Risk, Prevention, Injury, and Repair.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- A critical time window for the analgesic effect of central histamine in the partial sciatic ligation model of neuropathic pain.Journal of neuroinflammation · 2016Article
- Multifunctional Phosphorescent Conjugated Polymer Dots for Hypoxia Imaging and Photodynamic Therapy of Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2016Article
- Inhibition of G protein-coupled receptor 81 (GPR81) protects against ischemic brain injury.CNS neuroscience & therapeutics · 2015Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We hypothesized that activation of the central histaminergic system is required for neuroprotection induced by hypoxic preconditioning. Wild-type (WT) and histidine decarboxylase knockout (HDC-KO) mice were preconditioned by 3 hours of hypoxia (8% O(2)) and, 48 hours later, subjected to 30 minutes of middle cerebral artery (MCA) occlusion, followed by 24 hours of reperfusion. Hypoxic preconditioning improved neurologic function and decreased infarct volume in WT or HDC-KO mice treated with histamine, but not in HDC-KO or WT mice treated with α-fluoromethylhistidine (α-FMH, an inhibitor of HDC). Laser-Doppler flowmetry analysis showed that hypoxic preconditioning ameliorated cerebral blood flow (CBF) in the periphery of the MCA territory during ischemia in WT mice but not in HDC-KO mice. Histamine decreased in the cortex of WT mice after 2, 3, and 4 hours of hypoxia, and HDC activity increased after 3 hours of hypoxia. Vascular endothelial growth factor (VEGF) mRNA and protein expressions showed a greater increase after hypoxia than those in HDC-KO or α-FMH-treated WT mice. In addition, the VEGF receptor-2 antagonist SU1498 prevented the protective effect of hypoxic preconditioning in infarct volume and reversed increased peripheral CBF in WT mice. Therefore, endogenous histamine is an essential mediator of hypoxic preconditioning. It may function by enhancing hypoxia-induced VEGF expression.
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