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The Journal of Neuroscience, March 1, 2006, 26(9):2413-2418; doi:10.1523/JNEUROSCI.3680-05.2006

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Neurobiology of Disease
Fragile X Mental Retardation Protein Shifts between Polyribosomes and Stress Granules after Neuronal Injury by Arsenite Stress or In Vivo Hippocampal Electrode Insertion

Soong Ho Kim,^1,2 Willie K. Dong,¹ Ivan Jeanne Weiler,¹ and William T. Greenough^1,2,3

¹Beckman Institute, ²Neuroscience Program, and ³Departments of Psychology, Psychiatry, and Cell and Developmental Biology, University of Illinois at Urbana–Champaign, Urbana, Illinois 61801

Correspondence should be addressed to Soong Ho Kim, Beckman Institute, 405 North Mathews Avenue, Urbana, IL 61801. Email: kanai{at}uiuc.edu

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.

Key words: FMRP; stress granules; brain injury; protein translation; LTP; ischemia

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Received Aug. 31, 2005; revised Jan. 12, 2006; accepted Jan. 14, 2006.

Correspondence should be addressed to Soong Ho Kim, Beckman Institute, 405 North Mathews Avenue, Urbana, IL 61801. Email: kanai{at}uiuc.edu

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