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

Authors:
Philip Rosenstiel, Jobst Sievers, Ralph Lucius
Year of publication:
2002
Volume:
308
Issue:
2
Issn:
0302-766X
Journal title abbreviated:
CELL TISSUE RES
Journal title long:
Cell and tissue research
Impact factor:
2.948
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.