ArticleMolecular neurobiology2018
Hypoxia-Induced Neuroinflammation and Learning-Memory Impairments in Adult Zebrafish Are Suppressed by Glucosamine.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Article
- Brain-wide mapping of acute hypoxia-induced neuronal activation in mice: A c-Fos immunofluorescence study.IBRO neuroscience reports · 2025Article
- Cross-generational plasticity in Atlantic silversides (Menidia menidia) under the combined effects of hypoxia and acidification.The Journal of experimental biology · 2025Article
- Behavioral neuroscience in zebrafish: unravelling the complexity of brain-behavior relationships.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Multi-omics analysis reveals phenylalanine enhance mitochondrial function and hypoxic endurance via LKB1/AMPK activation.Journal of translational medicine · 2024Article
- Protective effect of increased O-GlcNAc cycling against 6-OHDA induced Parkinson's disease pathology.Cell death & disease · 2024Article
- Causality of genetically determined glucosamine supplementation on cognition and sarcopenia: a Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Repeated sleep deprivation decreases the flux into hexosamine biosynthetic pathway/O-GlcNAc cycling and aggravates Alzheimer's disease neuropathology in adult zebrafish.Journal of neuroinflammation · 2023Article
- Habitual glucosamine use, APOE genotypes, and risk of incident cause-specific dementia in the older population.Alzheimer's research & therapy · 2023Article
- Association of regular glucosamine use with incident dementia: evidence from a longitudinal cohort and Mendelian randomization study.BMC medicine · 2023Article
- Cyclooxygenase‑2 contributes to the hypoxia‑induced aggravation of the neuroinflammation response stimulated by lipopolysaccharide in microglia.Experimental and therapeutic medicine · 2023Article
- Causal associations between common musculoskeletal disorders and dementia: a Mendelian randomization study.Frontiers in aging neuroscience · 2023Article
- Animal Inflammation-Based Models of Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2023Article
- Neuroprotective and Proneurogenic Effects of Glucosamine in an Internal Carotid Artery Occlusion Model of Ischemia.Neuromolecular medicine · 2022Article
- Article
- Resetting Proteostasis of CIRBP with ISRIB Suppresses Neural Stem Cell Apoptosis under Hypoxic Exposure.Oxidative medicine and cellular longevity · 2022Article
- Pre-Exposure to Environmental Enrichment Protects against Learning and Memory Deficits Caused by Infrasound Exposure.Oxidative medicine and cellular longevity · 2022Article
- Insight into the Effects of High-Altitude Hypoxic Exposure on Learning and Memory.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
This study investigated changes in neuroinflammation and cognitive function in adult zebrafish exposed to acute hypoxia and protective effects of glucosamine (GlcN) against hypoxia-induced brain damage. The survival rate of zebrafish following exposure to hypoxia was improved by GlcN pretreatment. Moreover, hypoxia-induced upregulation of neuroglobin, NOS2α, glial fibrillary acidic protein, and S100β in zebrafish was suppressed by GlcN. Hypoxia stimulated cell proliferation in the telencephalic ventral domain and in cerebellum subregions. GlcN decreased the number of bromodeoxyuridine (BrdU)-positive cells in the telencephalon region, but not in cerebellum regions. Transient motor neuron defects, assessed by measuring the locomotor and exploratory activity of zebrafish exposed to hypoxia recovered quickly. GlcN did not affect hypoxia-induced motor activity changes. In passive avoidance tests, hypoxia impaired learning and memory ability, deficits that were rescued by GlcN. A learning stimulus increased the nuclear translocation of phosphorylated cAMP response element binding protein (p-CREB), an effect that was greatly inhibited by hypoxia. GlcN restored nuclear p-CREB after a learning trial in hypoxia-exposed zebrafish. The neurotransmitters, γ-aminobutyric acid and glutamate, were increased after hypoxia in the zebrafish brain, and GlcN further increased their levels. In contrast, acetylcholine levels were reduced by hypoxia and restored by GlcN. Acetylcholinesterase inhibitor physostigmine partially reversed the impaired learning and memory of hypoxic zebrafish. This study represents the first examination of the molecular mechanisms underlying hypoxia-induced memory and learning defects in a zebrafish model. Our results further suggest that GlcN-associated hexosamine metabolic pathway could be an important therapeutic target for hypoxic brain damage.
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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.