CYCLOHEXIMIDE PHASE-SHIFTS, BUT DOES NOT PREVENT, DE-NOVO KROX-24 PROTEIN EXPRESSION

PREVIOUS studies show that focal hippocampal injury transiently increa ses NMDA receptor-dependent expression of inducible transcription fact ors (ITFs including Krox-24) in rat dentate gyrus neurons. Furthermore , pretreatment with the protein synthesis inhibitor, cyclo-heximide (C HX), prevents de novo ITF protein expression 1 h post-injury. Here, we further characterize the effects of a single pretreatment dose of CHX on injury-induced expression of Krox-24 and show that CHX pretreatmen t phase-shifts (delays), but does not prevent, de novo expression of K rox-24 in hippocampal dentate gyrus neurons following injury. This may have implications for studies which use CHX pretreatment to examine t he role of gene expression and de novo protein synthesis in long-term memory formation, the stabilization of long-term potentiation, kindlin g and neuronal injury.