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Is fragile X mental retardation protein involved in activity-induced plasticity of dendritic spines?

作者信息

Segal Menahem, Kreher Ute, Greenberger Varda, Braun Katharina

机构信息

Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel.

出版信息

Brain Res. 2003 May 16;972(1-2):9-15. doi: 10.1016/s0006-8993(03)02410-7.

DOI:10.1016/s0006-8993(03)02410-7
PMID:12711073
Abstract

Dendritic morphology of 2-week-old cultured neurons, taken from postnatal day 1 fragile X mental retardation gene1 knock out (FMR1-/-) mice hippocampus, were compared with cells taken from wild type mice. Under control conditions the FMR1-/- neurons displayed significantly lower spine densities compared to wild type neurons. Pharmacological stimulation of electrical activity, induced by bicuculline, caused a reduction in dendritic spine density in both the FMR1-/- and the wild type cells. In both groups, bicuculline induced a significant shrinkage of spines that were occupied by one or more synaptophysin-immunoreactive presynaptic terminals. The concentration of FMR1 in the wild type cultures was not affected by bicuculline treatment. These experiments indicate that FMR1 is not likely to be an essential factor in activity-modulated morphological plasticity of dendritic spines in cultured hippocampal neurons.

摘要

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