Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity

被引:218
作者
Deller, T
Korte, M
Chabanis, S
Drakew, A
Schwegler, H
Stefani, GG
Zuniga, A
Schwarz, K
Bonhoeffer, T
Zeller, R
Frotscher, M
Mundel, P
机构
[1] Univ Freiburg, Inst Anat, D-79001 Freiburg, Germany
[2] Goethe Univ Frankfurt, Inst Clin Neuroanat, D-60590 Frankfurt, Germany
[3] Max Planck Inst Neurobiol, Dept Cellular & Syst Neurobiol, D-82152 Martinsried, Germany
[4] European Mol Biol Lab, D-69117 Heidelberg, Germany
[5] Heidelberg Univ, Dept Anat & Cell Biol, D-69120 Heidelberg, Germany
[6] Univ Magdeburg, Inst Anat, D-39120 Magdeburg, Germany
[7] Univ Utrecht, Fac Biol, Dept Dev Biol, NL-3584 CH Utrecht, Netherlands
[8] Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA
[9] Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10461 USA
关键词
D O I
10.1073/pnas.1832384100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The spine apparatus is a cellular organelle that is present in many dendritic spines of excitatory neurons in the mammalian forebrain. Despite its discovery >40 years ago, the function of the spine apparatus is still unknown although calcium buffering functions as well as roles in synaptic plasticity have been proposed. We have recently shown that the 100-kDa protein synaptopodin is associated with the spine apparatus. Here, we now report that mice homozygous for a targeted deletion of the synaptopodin gene completely lack spine apparatuses. Interestingly, this absence of the spine apparatus is accompanied by a reduction in hippocampal long-term potentiation (LTP) in the CA1 region of the hippocampus and by an impairment of spatial learning in the radial arm maze test. This genetic analysis points to a role of the spine apparatus in synaptic plasticity.
引用
收藏
页码:10494 / 10499
页数:6
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