ApoE receptor 2 regulates synapse and dendritic spine formation.
ApoE receptor 2 regulates synapse and dendritic spine formation.
复制标题
DOI:
10.1371/journal.pone.0017203
复制
发表时间:
2011-02-15
期刊:
影响因子:
3.7
通讯作者:
Hoe HS
中科院分区:
文献类型:
--
作者:
Dumanis SB;Cha HJ;Song JM;Trotter JH;Spitzer M;Lee JY;Weeber EJ;Turner RS;Pak DT;Rebeck GW;Hoe HS
Apolipoprotein E receptor 2 (ApoEr2) is a postsynaptic protein involved in long-term potentiation (LTP), learning, and memory through unknown mechanisms. We examined the biological effects of ApoEr2 on synapse and dendritic spine formation—processes critical for learning and memory. In a heterologous co-culture synapse assay, overexpression of ApoEr2 in COS7 cells significantly increased colocalization with synaptophysin in primary hippocampal neurons, suggesting that ApoEr2 promotes interaction with presynaptic structures. In primary neuronal cultures, overexpression of ApoEr2 increased dendritic spine density. Consistent with our in vitro findings, ApoEr2 knockout mice had decreased dendritic spine density in cortical layers II/III at 1 month of age. We also tested whether the interaction between ApoEr2 and its cytoplasmic adaptor proteins, specifically X11α and PSD-95, affected synapse and dendritic spine formation. X11α decreased cell surface levels of ApoEr2 along with synapse and dendritic spine density. In contrast, PSD-95 increased cell surface levels of ApoEr2 as well as synapse and dendritic spine density. These results suggest that ApoEr2 plays important roles in structure and function of CNS synapses and dendritic spines, and that these roles are modulated by cytoplasmic adaptor proteins X11α and PSD-95.
登录
查看更多内容
影响因子:
5.3
作者:
Hoe, Hyang-Sook;Cooper, Matthew J.;Rebeck, G. William
通讯作者:
Rebeck, G. William
影响因子:
3.3
作者:
Clatworthy, AE;Stockinger, W;Rebeck, GW
通讯作者:
Rebeck, GW
影响因子:
4.8
作者:
Biederer, T;Südhof, TC
通讯作者:
Südhof, TC
影响因子:
16.2
作者:
Dulabon, L;Olson, EC;Anton, ES
通讯作者:
Anton, ES
DOI:
10.1073/pnas.0308655100
发表时间:
2004-02-24
影响因子:
11.1
作者:
Ho, A;Südhof, TC
通讯作者:
Südhof, TC