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Activity-dependent dendritic spine structural plasticity is regulated by small GTPase Rap1 and its target AF-6
被引:97
作者:

Xie, Z
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机构: Northwestern Univ, Feinberg Sch Med, Dept Physiol, Chicago, IL 60611 USA

Huganir, RL
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机构: Northwestern Univ, Feinberg Sch Med, Dept Physiol, Chicago, IL 60611 USA

Penzes, P
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机构: Northwestern Univ, Feinberg Sch Med, Dept Physiol, Chicago, IL 60611 USA
机构:
[1] Northwestern Univ, Feinberg Sch Med, Dept Physiol, Chicago, IL 60611 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA
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D O I:
10.1016/j.neuron.2005.09.027
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
Activity-dependent remodeling of dendritic spines is essential for neural circuit development and synaptic plasticity, but the mechanisms that coordinate synaptic structural and functional plasticity are not well understood. Here we investigate the signaling pathways that enable excitatory synapses to undergo activity-dependent structural modifications. We report that activation of NMDA receptors in cultured cortical neurons induces spine morphogenesis and activation of the small GTPase Rap1. Rap1 bimodally regulates spine morphology: activated Rap1 recruits the PDZ domain-containing protein AF-6 to the plasma membrane and induces spine neck elongation, while inactive Rap1 dissociates AF-6 from the membrane and induces spine enlargement. Rap1 also regulates spine content of AMPA receptors: thin spines induced by Rap1 activation have reduced GluR1-containing AMPA receptor content, while large spines induced by Rap1 inactivation are rich in AMPA receptors. These results identify a signaling pathway that regulates activity-dependent synaptic structural plasticity and coordinates it with functional plasticity.
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页码:605 / 618
页数:14
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