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缺乏棘器和池状细胞器的突触素缺陷小鼠齿状回中体内θ波爆发式长时程增强和网络兴奋性受损。

Impairment of in vivo theta-burst long-term potentiation and network excitability in the dentate gyrus of synaptopodin-deficient mice lacking the spine apparatus and the cisternal organelle.

作者信息

Jedlicka Peter, Schwarzacher Stephan W, Winkels Raphael, Kienzler Friederike, Frotscher Michael, Bramham Clive R, Schultz Christian, Bas Orth Carlos, Deller Thomas

机构信息

Department of Clinical Neuroanatomy, Goethe-University of Frankfurt, Frankfurt am Main, Germany.

出版信息

Hippocampus. 2009 Feb;19(2):130-40. doi: 10.1002/hipo.20489.

DOI:10.1002/hipo.20489
PMID:18767067
Abstract

The function of the spine apparatus in dendritic spines and the cisternal organelles in axon initial segments is little understood. The actin-associated protein, synaptopodin, is essential for the formation of these organelles which are absent in synaptopodin -/- mice. Here, we used synaptopodin -/- mice to explore the role of the spine apparatus and the cisternal organelle in synaptic plasticity and local circuit excitability in response to activation of the perforant path input to the dentate gyrus in vivo. We found impaired long-term potentiation following theta-burst stimulation, whereas tetanus-evoked LTP was unaffected. Furthermore, paired-pulse inhibition of the population spike was reduced and granule cell excitability was enhanced in mutants, hence revealing an impairment of local network inhibition. In summary, our data represent the first electrophysiological evidence that the lack of the spine apparatus and the cisternal organelle leads to a defect in long-term synaptic plasticity and alterations in local circuit control of granule cell excitability under adult in vivo conditions.

摘要

树突棘中脊柱装置以及轴突起始段中池状细胞器的功能鲜为人知。肌动蛋白相关蛋白突触素对于这些细胞器的形成至关重要,而在突触素基因敲除小鼠中则不存在这些细胞器。在此,我们使用突触素基因敲除小鼠来探究脊柱装置和池状细胞器在体内对齿状回穿通通路输入激活的突触可塑性和局部回路兴奋性中的作用。我们发现,在theta爆发刺激后长时程增强受损,而强直刺激诱发的长时程增强不受影响。此外,在突变体中群体峰电位的配对脉冲抑制降低,颗粒细胞兴奋性增强,从而揭示了局部网络抑制的损伤。总之,我们的数据代表了首个电生理证据,即在成年体内条件下,缺乏脊柱装置和池状细胞器会导致长期突触可塑性缺陷以及颗粒细胞兴奋性局部回路控制的改变。

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