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PMID:16087343
| Citation |
Asaka, Y, Jugloff, DG, Zhang, L, Eubanks, JH and Fitzsimonds, RM (2006) Hippocampal synaptic plasticity is impaired in the Mecp2-null mouse model of Rett syndrome. Neurobiol. Dis. 21:217-27 |
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| Abstract |
Rett syndrome is an X-linked neurodevelopmental disorder caused by mutations in the gene encoding the transcriptional repressor methyl-CpG-binding protein 2 (MeCP2). Here we demonstrate that the Mecp2-null mouse model of Rett syndrome shows an age-dependent impairment in hippocampal CA1 long-term potentiation induced by tetanic or theta-burst stimulation. Long-term depression induced by repetitive low-frequency stimulation is also absent in behaviorally symptomatic Mecp2-null mice. Immunoblot analyses from behaviorally symptomatic Mecp2-null mice reveal altered expression of N-methyl-d-aspartate receptor subunits NR2A and NR2B. Presynaptic function is also affected, as demonstrated by a significant reduction in paired-pulse facilitation. Interestingly, the properties of basal neurotransmission are normal in the Mecp2-null mice, consistent with our observations that the levels of expression of synaptic and cytoskeletal proteins, including glutamate receptor subunits GluR1 and GluR2, PSD95, synaptophysin-1, synaptobrevin-2, synaptotagmin-1, MAP2, betaIII-tubulin and NF200, are not significantly altered. Together, these data provide the first evidence that the loss of Mecp2 expression is accompanied by age-dependent alterations in excitatory synaptic plasticity that are likely to contribute to the cognitive and functional deficits underlying Rett syndrome. |
| Links |
PubMed Online version:10.1016/j.nbd.2005.07.005 |
| Keywords |
Animals; Cytoskeletal Proteins/metabolism; Disease Models, Animal; Excitatory Postsynaptic Potentials/physiology; Hippocampus/physiology; Long-Term Potentiation/physiology; Methyl-CpG-Binding Protein 2/genetics; Methyl-CpG-Binding Protein 2/metabolism; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Neuronal Plasticity/physiology; Receptors, N-Methyl-D-Aspartate/metabolism; Rett Syndrome/metabolism; Rett Syndrome/physiopathology; Synaptic Transmission/physiology; Theta Rhythm |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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