Modulation of GFAP mRNA levels following toxic lesions in the basal ganglia of the rat.

GFAP mRNA levels were quantified by Northern blot analysis using a human GFAP (glial fibrillary acidic protein) cDNA probe in association with immunocytochemistry. Ten days after a unilateral lesion of substantia nigra with 6-hydroxydopamine (6-OHDA), GFAP mRNA level is increased 1.4-fold in the ipsilateral striatum; thereafter it declined continuously to reach the control level 4 months later. This effect contrasted with the lower and more sustained increase of preproenkephalin (PPE) mRNA, a marker of neuronal target of nigrostriatal pathway. Following ibotenic acid-induced neuronal degeneration of the neostriatum in the rat, we observed a sharp elevation of the GFAP transcripts (4-fold) as soon as 2 days after the lesion both in the striatum and in the substantia nigra. Whereas in the striatum GFAP mRNA level already declined at 5 days postlesion, it remained stable in the substantia nigra. In comparison GFAP immunoreactivity was slightly delayed. No obvious modification was observed in the contralateral side to the lesion whatever the denervation condition studied. Implication of these results on the understanding and the therapeutic approach of glial scarring is discussed.