Deficient development and maintenance of postsynaptic specializations in mutant mice lacking an 'adult' acetylcholine receptor subunit

被引:0
|
作者
Missias, AC
Mudd, J
Cunningham, JM
Steinbach, JH
Merlie, JP
Sanes, JR [1 ]
机构
[1] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Dept Anesthesiol, St Louis, MO 63110 USA
来源
DEVELOPMENT | 1997年 / 124卷 / 24期
关键词
acetylcholine receptor; neuromuscular junction; synapse formation; mouse;
D O I
暂无
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
At many synapses, 'fetal' neurotransmitter receptor subunits are replaced by 'adult' subunits as development proceeds. To assess the significance of such transitions, we deleted the gene encoding the adult acetylcholine receptor (AChR) epsilon subunit, which replaces its fetal counterpart, the gamma subunit, at the skeletal neuromuscular junction during early postnatal life. Several aspects of postnatal maturation, including synapse elimination, proceeded normally in the absence of the adult AChR, but structural development of the endplate was compromised. Later, inadequate compensation by the gamma subunit led to severely reduced AChR density in mutant endplates relative to controls. This decreased density led to a profound reorganization of AChR-associated components of the postsynaptic membrane and cytoskeleton. Together, these results suggest novel roles for AChRs in assembly of the postsynaptic apparatus.
引用
收藏
页码:5075 / 5086
页数:12
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