NEUROTOXIC INJURY IN RAT HIPPOCAMPUS DIFFERENTIALLY AFFECTS MULTIPLE TRKB AND TRKC TRANSCRIPTS

In the present work we determined, by Northern blotting, ribonuclease assay and in situ hybridization, the level of multiple trkB and trkC t ranscripts at different times after ibotenic acid-induced neuronal inj ury in the rat hippocampus. All the transcripts (7.0-7.5, 2.4 and 1.8 kb) encoding the truncated TrkB receptor are coordinately up-regulated following neurotoxic injury, with a time-course similar to that obser ved for the glial fibrillary acidic protein mRNA, a molecular marker o f reactive astrocytes. The highest level of induction was observed for the 2.4 kb mRNA level. The 1.8 kb mRNA, whose relative level is highe r in astroglial cultures compared to normal brain tissue, is detectabl e only in the gliotic hippocampus. The 9 kb trkB mRNA, which encodes t he full-length TrkB receptor, rapidly decreases with a time-course sim ilar to that previously observed for other neuronal markers. In situ h ybridization studies show that the increased mRNA level per cell is a major determinant in the up-regulation of truncated trkB expression. A decrease of truncated and full-length trkC mRNA was observed in the n euron-depleted astroglia-enriched hippocampus, suggesting that this mR NA is mainly localized in the neuronal layers and that no induction of its expression occurs in reactive astrocytes.