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The Journal of Neuroscience, November 15, 2002, 22(22):9810-9820

Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine

Olivier Braissant^{1, *}, Hugues Henry^{1, *}, Anne-Marie Villard¹, Marie-Gabrielle Zurich², Marc Loup¹, Barbara Eilers¹, Gianni Parlascino¹, Edouard Matter¹, Olivier Boulat¹, Paul Honegger², and Claude Bachmann¹

¹ Clinical Chemistry Laboratory, University Hospital, CH-1011 Lausanne, Switzerland, and ² Institute of Physiology, University of Lausanne, CH-1005 Lausanne, Switzerland

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.

Key words: hyperammonemia; axon; creatine; glia; neurofilament; phosphorylation

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^* O.B. and H.H. contributed equally to this work.

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22229810-11$05.00/0

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