Sensory stimulation increases cortical expression of the fragile X mental retardation protein in vivo.
Brain Res Mol Brain Res
; 80(1): 17-25, 2000 Aug 14.
Article
em En
| MEDLINE
| ID: mdl-11039725
ABSTRACT
Fragile X syndrome is a common cause of mental retardation that results from the absence of the fragile X mental retardation protein (FMRP), an RNA binding protein whose function remains unclear. Recent in vitro work has demonstrated that the protein is translated near the synapse in an activity dependent manner [33]. We therefore asked whether expression of FMRP might be altered by neuronal activity in vivo. Using immunoblots of different sub-cellular fractions of the rat somatosensory cortex, we show that the levels of FMRP increase significantly following unilateral whisker stimulation, a model of experience dependent plasticity. This increase is greatest between 2 and 8 h after the stimulus and is seen in both a synaptosomal fraction as well as a sub-cellular fraction enriched for polyribosomal complexes. In contrast, detectable levels of FMRP within the somatosensory cortex show either a decrease or no change after a kainic acid induced seizure compared to water treated controls. Our findings demonstrate that FMRP expression levels are modulated in vivo in response to neuronal activity and suggest a role for FMRP in activity dependent plasticity.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Limiar Sensorial
/
Proteínas de Ligação a RNA
/
Síndrome do Cromossomo X Frágil
/
Deficiência Intelectual
/
Proteínas do Tecido Nervoso
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Brain Res Mol Brain Res
Assunto da revista:
BIOLOGIA MOLECULAR
/
CEREBRO
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Estados Unidos