Neuroscience 2001 Abstract
| Presentation Number: | 670.3 |
|---|---|
| Abstract Title: | Some translational deficits in fmr-1 KO mice. |
| Authors: |
Weiler, I. J.*1
; Lin, L.1
; Belt, B.1
; Greenough, W. T.1
1Beckman Institute, University of Illinois, U-C, Urbana, IL |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Developmental Disorders -- Genetic |
| Session: |
670. Developmental disorders: genetic I Poster |
| Presentation Time: | Tuesday, November 13, 2001 3:00 PM-4:00 PM |
| Location: | Exhibit Hall BBB-15 |
| Keywords: | mGluR1, synaptic plasticity, Fragile X, glutamate receptor |
A protein (FMRP) which is lacking in patients with Fragile X Mental Retardation is also not produced in fmr-1 KO mice, a model for the syndrome. In previous work, we showed that fmr-1 KO mice do not initiate increased synaptic translation in response to glutamate neurotransmitter stimulation (Spangler et al., SfN 1998). Moreover, these KO mice exhibit lower numbers of polyribosomes in postsynaptic spines. Thus the absence of FMRP seems to be associated with a translational defect; it seems likely that a specific subset of proteins might be affected .
We have used Western blots of proteins from synaptoneurosomes from 3 brain areas (cortex, cerebellum, hippocampus) of mice aged 6 days to 4 weeks, to compare levels of glutamate receptors and other proteins during development. Each of the synaptic proteins tested (AMPA receptors GluR1, GluR1; mGluR1; GABA A) is present, on average, at slightly lower levels in KO cortex than in WT cortex, in young mice. There is a particularly striking cortical deficit in mGluR1. This deficit is not observed in the cerebellum and is milder in the hippocampus. Downregulation of mGluR1 might impinge on the ability of cortical synapses to remodel rapidly, since we have shown that mGluR1 receptors trigger the rapid translational response.
We have used Western blots of proteins from synaptoneurosomes from 3 brain areas (cortex, cerebellum, hippocampus) of mice aged 6 days to 4 weeks, to compare levels of glutamate receptors and other proteins during development. Each of the synaptic proteins tested (AMPA receptors GluR1, GluR1; mGluR1; GABA A) is present, on average, at slightly lower levels in KO cortex than in WT cortex, in young mice. There is a particularly striking cortical deficit in mGluR1. This deficit is not observed in the cerebellum and is milder in the hippocampus. Downregulation of mGluR1 might impinge on the ability of cortical synapses to remodel rapidly, since we have shown that mGluR1 receptors trigger the rapid translational response.
Supported by Supported by FRAXA Research Foundation, Illinois-Eastern Iowa District of Kiwanis International Spastic Paralysis Research Foundation, and NICHD RO3-64272.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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