(-)-Deprenyl fails to promote axonal regeneration of retinal ganglion cells in vitro and in vivo

Cell Tissue Res. 2002 May;308(2):167-75. doi: 10.1007/s00441-002-0551-x. Epub 2002 Apr 26.

Abstract

(-)-Deprenyl ( L-deprenyl, selegiline hydrochloride), a selective monoamine oxidase B (MAO-B) inhibitor employed in the pharmacological therapy of Parkinson's disease, increases neuronal survival in both animal models of neurodegenerative disorders and acute CNS lesions. Despite intensive investigations, the mechanisms of (-)-deprenyl-mediated neuroprotection remain poorly understood. To test the hypothesis that (-)-deprenyl might have a beneficial effect not only on neuronal survival, but also on axonal regeneration, we describe here experiments performed in vitro and in vivo which clearly demonstrate that (-)-deprenyl fails to promote axonal regeneration of severed rat retinal ganglion cells (RGCs). Furthermore, (-)-deprenyl was not able to overcome free-radical-induced RGC axon degeneration. These results challenge the notion that (-)-deprenyl might be useful as a monotherapy for acute CNS lesions and give rise to a more critical viewpoint of the trophic-like function of this widely used therapeutic agent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / drug effects*
  • Brain-Derived Neurotrophic Factor / pharmacology
  • Cell Survival / drug effects
  • Free Radicals / toxicity
  • GAP-43 Protein / biosynthesis
  • Ganglia, Spinal / cytology
  • Ganglia, Spinal / drug effects
  • Ganglia, Spinal / growth & development
  • Gene Expression Regulation / drug effects
  • Genes, bcl-2 / genetics
  • Immunohistochemistry
  • In Vitro Techniques
  • Male
  • Molsidomine / analogs & derivatives*
  • Molsidomine / pharmacology
  • Monoamine Oxidase Inhibitors / pharmacology*
  • Nerve Degeneration / chemically induced
  • Nerve Degeneration / prevention & control
  • Nerve Regeneration / drug effects*
  • Neurites / drug effects
  • Neuroprotective Agents / pharmacology*
  • Optic Nerve / cytology
  • Optic Nerve / drug effects
  • Oxidative Stress / drug effects
  • Rats
  • Rats, Wistar
  • Receptor, trkA / biosynthesis
  • Receptor, trkB / biosynthesis
  • Retinal Ganglion Cells / drug effects*
  • Selegiline / pharmacology*

Substances

  • Brain-Derived Neurotrophic Factor
  • Free Radicals
  • GAP-43 Protein
  • Monoamine Oxidase Inhibitors
  • Neuroprotective Agents
  • Selegiline
  • linsidomine
  • Molsidomine
  • Receptor, trkA
  • Receptor, trkB