Cadherin activity is required for activity-induced spine remodeling.
Cadherin activity is required for activity-induced spine remodeling.
批准号:
15590226
负责人:
TANAKA Hidekazu
金额:
$2.3万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004
中文摘要
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英文摘要
Neural activity induces the remodeling of pre- and postsynaptic membranes, which maintain their apposition through cell adhesion molecules. Among them, N-cadherin is redistributed, undergoes activity-dependent conformational changes, and is required for synaptic plasticity. Here we show that depolarization induces the enlargement of the width of spine head, and that cadherin activity is essential for this synaptic rearrangement. Dendritic spines visualized with green fluorescent protein in hippocampal neurons showed an expansion by the activation of AMPA receptor, so that the synaptic apposition zone may be expanded. N-cadherin-venus fusion protein laterally dispersed along the expanding spine head. Overexpression of dominant-negative forms of N-cadherin resulted in the abrogation of the spine expansion. Inhibition of actin polymerization with cytochalasin D abolished the spine expansion. Taken together, our data suggest that cadherin-based adhesion machinery coupled with the actin-cytoskeleton is critical for the remodeling of synaptic apposition zone.
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Gamma-protocadherins are targeted to subsets of synapses and intracellular organelles in neurons.
γ-原钙粘蛋白靶向神经元中的突触子集和细胞内细胞器。
DOI:
--
发表时间:
2003
期刊:
J Neurosci. 23
影响因子:
--
作者:
[Phillips GR, et al.]
通讯作者:
et al.
DOI:
10.1172/jci200420622
发表时间:
2004-08-01
期刊:
JOURNAL OF CLINICAL INVESTIGATION
影响因子:
15.9
作者:
[Taguchi, A, Soma, T, Matsuyama, T]
通讯作者:
Matsuyama, T
Kumamaru-E et al.: "Reticulon3 expression in rat optic and olfactory systems"Neurosci.Lett.. 356. 17-20 (2004)
Kumamaru-E 等人:“大鼠视神经和嗅觉系统中的 Reticulon3 表达”Neurosci.Lett.. 356. 17-20 (2004)
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
DOI:
10.1083/jcb.200406030
发表时间:
2004-12-06
期刊:
JOURNAL OF CELL BIOLOGY
影响因子:
7.8
作者:
[Okamura, K, Tanaka, H, Miki, N]
通讯作者:
Miki, N
Molecular cloning and characterization of rKAB1, which interacts With KARP-1, localizes in the nucleus and protects cell against oxidative death.
rKAB1 的分子克隆和表征,它与 KARP-1 相互作用,定位于细胞核并保护细胞免遭氧化死亡。
DOI:
--
发表时间:
2003
期刊:
Mol.Cell.Biochem. 248
影响因子:
--
作者:
[E.Do, et al.]
通讯作者:
et al.
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