Neuro-protective effects of increased O-GlcNAcylation by glucosamine in an optic tectum traumatic brain injury model of adult zebrafish.

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  • Additional Information
    • Source:
      Publisher: Oxford University Press Country of Publication: England NLM ID: 2985192R Publication Model: Print Cited Medium: Internet ISSN: 1554-6578 (Electronic) Linking ISSN: 00223069 NLM ISO Abbreviation: J Neuropathol Exp Neurol Subsets: MEDLINE
    • Publication Information:
      Publication: 2016- : Oxford, England : Oxford University Press
      Original Publication: Lawrence, Ks : Association of the journal of neuropathology and experimental neurology
    • Subject Terms:
      Zebrafish* ; Glucosamine*/pharmacology ; Brain Injuries, Traumatic*/metabolism ; Brain Injuries, Traumatic*/pathology ; Superior Colliculi*/drug effects ; Superior Colliculi*/metabolism ; Disease Models, Animal*; Animals ; N-Acetylglucosaminyltransferases/metabolism ; Neuroprotective Agents/pharmacology
    • Abstract:
      This study investigated the behavioral and molecular changes in the telencephalon following needle stab-induced injury in the optic tectum of adult zebrafish. At 3 days post-injury (dpi), there was noticeable structural damage to brain tissue and reduced neuronal proliferation in the telencephalon that persisted until 30 dpi. Neurobehavioral deficits observed at 3 dpi included decreased exploratory and social activities and impaired learning and memory (L/M) functions; all of these resolved by 7 dpi. The injury led to a reduction in telencephalic phosphorylated cAMP response element-binding protein and O-GlcNAcylation, both of which were restored by 30 dpi. There was an increase in GFAP expression and nuclear translocation of NF-κB p65 at 3 dpi, which were not restored by 30 dpi. The injury caused decreased O-GlcNAc transferase and increased O-GlcNAcase levels at 3 dpi, normalizing by 30 dpi. Glucosamine (GlcN) treatment at 3 dpi significantly restored O-GlcNAcylation levels and L/M function, also reducing GFAP activation. Glucose treatment recovered L/M function by 7 dpi, but inhibition of the hexosamine biosynthetic pathway by 6-diazo-5-oxo-L-norleucine blocked this recovery. These findings suggest that the O-GlcNAc pathway is a potential therapeutic target for addressing L/M impairment following traumatic brain injury in zebrafish.
      (© The Author(s) 2024. Published by Oxford University Press on behalf of American Association of Neuropathologists, Inc. All rights reserved. For permissions, please email: [email protected].)
    • Grant Information:
      RS-2024-00346770 National Research Foundation; National Research Foundation; RS-2024-00346770 NRF; Inha University
    • Contributed Indexing:
      Keywords: O-GlcNAc transferase; brain injury; cognition; glucosamine
    • Accession Number:
      N08U5BOQ1K (Glucosamine)
      EC 2.4.1.- (N-Acetylglucosaminyltransferases)
      0 (Neuroprotective Agents)
      EC 2.4.1.- (O-GlcNAc transferase)
    • Publication Date:
      Date Created: 20240816 Date Completed: 20241018 Latest Revision: 20241022
    • Publication Date:
      20241023
    • Accession Number:
      10.1093/jnen/nlae092
    • Accession Number:
      39150431