Journal
HIPPOCAMPUS
Volume 22, Issue 2, Pages 241-254Publisher
WILEY-BLACKWELL
DOI: 10.1002/hipo.20890
Keywords
dentate gyrus; fragile X syndrome; synapse; long-term potentiation; long-term depression
Categories
Funding
- Vancouver Coastal Health-CIHR-UBC
- NSERC-CGS
- SRCFC
- FXRFC
- CIHR
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Fragile X syndrome (FXS) is the most common form of inherited intellectual disability in humans. This X-linked disorder is caused by the transcriptional repression of a single gene, Fmr1. The loss of Fmr1 transcription prevents the production of Fragile X mental retardation protein (FMRP) which in turn disrupts the expression of a variety of key synaptic proteins that appear to be important for intellectual ability. A clear link between synaptic dysfunction and behavioral impairment has been elusive, despite the fact that several animal models of FXS have been generated. Here we report that Fmr1 knockout mice exhibit impaired bidirectional synaptic plasticity in the dentate gyrus (DG) of the hippocampus. These deficits are associated with a novel decrease in functional NMDARs (N-methyl-D-aspartate receptors). In addition, mice lacking the Fmr1 gene show impaired performance in a context discrimination task that normally requires functional NMDARs in the DG. These data indicate that Fmr1 deletion results in significant NMDAR-dependent electrophysiological and behavioral impairments specific to the DG. (C) 2010 Wiley Periodicals, Inc.
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