缺乏突触足蛋白的小鼠没有棘器，并且在突触可塑性方面表现出缺陷。
Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity.
作者信息
Deller Thomas, Korte Martin, Chabanis Sophie, Drakew Alexander, Schwegler Herbert, Stefani Giulia Good, Zuniga Aimee, Schwarz Karin, Bonhoeffer Tobias, Zeller Rolf, Frotscher Michael, Mundel Peter
机构信息
Institute of Anatomy, University of Freiburg, P.O. Box 111, D-79001 Freiburg, Germany.
出版信息
Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10494-9. doi: 10.1073/pnas.1832384100. Epub 2003 Aug 19.
Abstract
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.
摘要
脊柱装置是一种细胞器，存在于哺乳动物前脑兴奋性神经元的许多树突棘中。尽管它在40多年前就被发现了，但脊柱装置的功能仍然未知，不过有人提出它有钙缓冲功能以及在突触可塑性中的作用。我们最近发现，100 kDa的蛋白质突触素与脊柱装置有关。在此，我们现在报告，突触素基因靶向缺失的纯合子小鼠完全没有脊柱装置。有趣的是，脊柱装置的缺失伴随着海马体CA1区海马体长期增强（LTP）的降低以及放射状臂迷宫试验中空间学习的受损。这种基因分析表明脊柱装置在突触可塑性中起作用。
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