ASTROCYTES UP-REGULATE GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP), BUT NOT INSULIN-LIKE GROWTH-FACTOR-I (IGF-I) DURING EXPERIMENTAL AUTOIMMUNE NEURITIS (EAN)

T cell-mediated autoimmune neuritis produces rapid activation of spina l cord microglia. To determine whether this microglial response upregu lates astrocytic expression of IGF-related proteins, we induced EAN an d used in situ hybridization and immunocytochemistry to examine the mR NAs and peptides for glial fibrillary acidic protein (GEAR), insulin-l ike growth factor-I (IGF-I), IGF-I receptor (IGFR-I) and IGF binding p rotein-2 (IGFBP-2). Relative levels of GFAP mRNA and peptide were high est in the lumbar spinal cord 4-10 d following T cell transfer and sig nificant GFAP elevations were still present after three weeks. The ast rocytes expressing GEAR mRNA and peptide were localized around motoneu rons which were related topographically to axons in peripheral nerve i nflammatory lesions. In the nucleus gracilis, where terminals of dorsa l root ganglion neurons are located, astrocytic levels of GFAP mRNA an d peptide rose later and did not reach their highest levels until 21 d after T cell transfer. Even though microglia were activated in both l ocations 2-4 d after transfer, astrocytic levels of IGF-I, IGFR-I and IGFBP-2 mRNA and peptide did not differ significantly from those obser ved in controls. The dissociation of GFAP and IGF-I expression in EAN suggests that these astrocytic responses may be independently regulate d. We also suggest that the type and severity of remote neuronal injur y are probably more important inducers and regulators of these astrocy tic responses than microglial cell activation.