Cerebral Cortex Advance Access originally published online on April 22, 2009
Cerebral Cortex 2009 19(7):1490-1492; doi:10.1093/cercor/bhp089
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Fragile X Mental Retardation Protein in the Driver's Seat
Department of Cell and Developmental Biology and Neuroscience Center, UNC Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA
Address correspondence to Dr Jay E. Brenman. Email: brenman@med.unc.edu.
Key Words: autism FMRP fmr1 Fragile X GABA mental retardation mGluR5
| The first 10% of the full text of this article appears below. |
Fragile X syndrome (FXS), the most common single gene cause of mental retardation, is securely associated with mutations in the fragile X mental retardation 1 gene, FMR1 (Fu et al. 1991
; Verkerk et al. 1991
; Feng et al. 1997
; Musumeci et al. 1999
; Hagerman et al. 2009
). Nevertheless, identification of consequences of loss of the protein product of FMR1, the fragile X mental retardation protein FMRP, has proven difficult. In this issue of Cerebral Cortex, 2 papers, one by Curia et al. and the other by Qiu et al., demonstrate that FMRP normally navigates the treacherous road of hippocampal excitation and inhibition, controlling the
-aminobutyric acidergic (GABAergic) brakes and glutamatergic
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