Ammonium-induced impairment of axonal growth is prevented through glial creatine.

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Date

15 novembre 2002

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Périmètre
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Source

Serveur académique Lausannois

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Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/12427837

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1529-2401

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_5EC36D0C3C269

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Serveur Académique Lausannois

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Université de Lausanne et CHUV

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info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer

Mots-clés 0

Adenosine Diphosphate/metabolism; Adenosine Monophosphate/metabolism; Adenosine Triphosphate/metabolism; Ammonium Chloride/toxicity; Animals; Axons/drug effects; Axons/metabolism; Axons/physiology; Cell Differentiation/physiology; Cell Division/drug effects; Cells, Cultured; Choline O-Acetyltransferase/biosynthesis; Coculture Techniques; Creatine/metabolism; Creatine/pharmacology; Dose-Response Relationship, Drug; GAP-43 Protein/biosynthesis; Glucose/pharmacokinetics; Immunohistochemistry; Intracellular Fluid/metabolism; Lactic Acid/metabolism; Neurofilament Proteins/biosynthesis; Neuroglia/cytology; Neuroglia/metabolism; Neurons/cytology; Neurons/drug effects; Neurons/metabolism; Phosphocreatine/metabolism; Quaternary Ammonium Compounds/pharmacokinetics; Rats; Telencephalon/cytology; Telencephalon/embryology

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Kreatine

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O. Braissant et al., « Ammonium-induced impairment of axonal growth is prevented through glial creatine. », Serveur académique Lausannois, ID : 10670/1.x35055

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Hyperammonemia in neonates and infants affects brain development and causes mental retardation. We report that ammonium impaired cholinergic axonal growth and altered localization and phosphorylation of intermediate neurofilament protein in rat reaggregated brain cell primary cultures. This effect was restricted to the phase of early maturation but did not occur after synaptogenesis. Exposure to NH4Cl decreased intracellular creatine, phosphocreatine, and ADP. We demonstrate that creatine cotreatment protected axons from ammonium toxic effects, although this did not restore high-energy phosphates. The protection by creatine was glial cell-dependent. Our findings suggest that the means to efficiently sustain CNS creatine concentration in hyperammonemic neonates and infants should be assessed to prevent impairment of axonogenesis and irreversible brain damage.

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