Reduction in glial fibrillary acidic protein mRNA abundance induced by (-)-deprenyl and other monoamine oxidase B inhibitors in C6 glioma cells.

Abstract

Gliosis is commonly observed in the CNS following tissue damage, and it also occurs in aging and in many neurodegenerative diseases. Glial fibrillary acidic protein (GFAP) accumulation is a prominent feature of astrocytic gliosis. An inhibition or delay in GFAP synthesis could mitigate scar formation and thus reduce the formation of a physical barrier. The consequence of this would be to allow neurons and oligodendrocytes to reestablish a functional environment. (-)-Deprenyl, a specific monoamine oxidase (MAO) B inhibitor, has been used as an effective antiparkinsonian drug, and it has been reported to possess neuroprotective and neurorescue properties. Using northern and slot blots to detect GFAP mRNA in C6 glioma cells, we have demonstrated that (-)-deprenyl decreases the abundance of GFAP mRNA in a time- and dose-dependent manner. The effect seems to be specific to MAO B inhibitors because (+)-deprenyl and clorgyline exhibit no effect. This study indicates therefore that (-)-deprenyl may be useful for regulating astrogliosis following CNS injury as well as in some neurodegenerative diseases.