Molecular NeuroscienceCycloheximide phase-shifts, but does not prevent, de novo Krox-24 protein expressionHughes, Paul E.1,3; Alexi, Tajrena1; Dragunow, Michael2Author Information 1Research Centre for Developmental Medicine and Biology (RCDMB), School of Medicine, The University of Auckland, Private Bag 92019, Auckland, New Zealand 2Department of Pharmacology and Clinical Pharmacology, School of Medicine, The University of Auckland, Private Bag 92019, Auckland, New Zealand 3Corresponding Author: Paul E. Hughes ACKNOWLEDGEMENTS: This research was supported by grants from the Neurological Foundation and Health Research Council of New Zealand to M.D. P.E.H. is a Health Research Council of New Zealand Senior Post-Doctoral Fellow. Website publication 29 September 1997 Received 18 July 1997; accepted 27 August 1997 NeuroReport: October 20th, 1997 - Volume 8 - Issue 15 - p 3263-3266 Buy Abstract PREVIOUS studies show that focal hippocampal injury transiently increases NMDA receptor-dependent expression of inducible transcription factors (ITFs including Krox-24) in rat dentate gyrus neurons. Furthermore, pretreatment with the protein synthesis inhibitor, cycloheximide (CHX), prevents de novo ITF protein expression 1 h post-injury. Here, we further characterize the effects of a single pretreatment dose of CHX on injuryinduced expression of Krox-24 and show that CHX pretreatment phase-shifts (delays), but does not prevent, de novo expression of Krox-24 in hippocampal dentate gyrus neurons following injury. This may have implications for studies which use CHX pretreatment to examine the role of gene expression and de novo protein synthesis in long-term memory formation, the stabilization of long-term potentiation, kindling and neuronal injury. © Lippincott-Raven Publishers.