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Up‐regulation of genes involved in cellular stress and apoptosis in a rat model of hippocampal degeneration

Changes in gene expression within the hippocampus induced by denervation after electrolytic fimbria‐fornix lesion in rat were compared to morphological and biochemical alterations. Fimbria‐fornix lesion results in degeneration of hippocampal cholinergic terminals as evidenced by a sustained (2 days to1 month) decrease in cholineacetyltransferase (ChAT) activity (50%). These changes were accompanied by a decrease in growth associated protein 43 (GAP‐43) immunoreactivity in all hippocampal layers 4 days after lesion followed by a subsequent increase and return to normal levels by 20 days postinjury. This increase in GAP‐43 expression in the hippocampus between 7 to 20 days after lesion may reflect heterotypic sprouting. TUNEL‐positive cells were revealed by in situ assay within the hippocampus at 10 days, but not at 3 days, after lesion. Two subtracted cDNA libraries from the dorsal hippocampus of control and injured rats (at 3 and 10 days postlesion) were constructed in order to search for new genes potentially implicated in degeneration/regeneration phenomena. We analysed 1,536 clones from each library by differential screening and found a total of 46 up‐regulated genes. Among the 15 known genes, 6 coded for proteins involved in signal transduction pathways. The up‐regulation of growth arrest DNA damage induced gene (GADD153), brain‐specific RING finger protein, JNK interacting protein (JIP‐1), protein kinase A (PKA), and Na+K+ ATPase was studied by quantitative polymerase chain reaction (PCR). Two of these genes, GADD153 and JIP‐1, have been previously shown to participate in cell modifications induced by stress and apoptosis. J. Neurosci. Res. 59:209–217, 2000 © 2000 Wiley‐Liss, Inc.