RT Journal Article SR Electronic T1 Fragile X Mental Retardation Protein Shifts between Polyribosomes and Stress Granules after Neuronal Injury by Arsenite Stress or In Vivo Hippocampal Electrode Insertion JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 2413 OP 2418 DO 10.1523/JNEUROSCI.3680-05.2006 VO 26 IS 9 A1 Soong Ho Kim A1 Willie K. Dong A1 Ivan Jeanne Weiler A1 William T. Greenough YR 2006 UL http://www.jneurosci.org/content/26/9/2413.abstract AB Fragile X mental retardation protein (FMRP), the lack of which causes fragile X syndrome, is an RNA-binding protein encoded by the FMR1 gene. FMRP accompanies mRNAs from the nucleus to dendritic regions and is thought to regulate their translation at synapses. It has been shown that FMRP moves into nontranslating stress granules (SGs) during heat stress of cultured fibroblasts (Mazroui et al., 2002). We used a novel method to isolate SGs from neurons by virtue of their TIA-1 (T-cell intracellular antigen 1) protein component, and found that FMRP moved out of polyribosomes and into SGs subsequent to oxidative stress. We then examined FMRP changes in subcellular localization resulting from mechanically induced neuronal injury by placement of electrodes into the dentate gyrus and the perforant path of the hippocampus in vivo. During the first 10 min after electrode insertion into one hippocampus, FMRP shifted into SGs and away from polyribosomes, in both hippocampi. Although the injury discharge subsided beyond 10 s, FMRP levels in polyribosomes and stress granules did not return to basal levels until 30 min after electrode penetration. Our findings suggest that procedures for in vivo induction of long-term potentiation or long-term depression should incorporate a 30 min rest period after electrode insertion, and indicate that the contralateral hippocampus cannot be considered an unstimulated control tissue.