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内嗅皮质损伤后大鼠齿状回中突触素和棘器细胞器的可塑性。

Plasticity of synaptopodin and the spine apparatus organelle in the rat fascia dentata following entorhinal cortex lesion.

作者信息

Deller Thomas, Bas Orth Carlos, Vlachos Andreas, Merten Tobias, Del Turco Domenico, Dehn Doris, Mundel Peter, Frotscher Michael

机构信息

Institute of Clinical Neuroanatomy, J.W. Goethe-University, D-60590 Frankfurt/Main, Germany.

出版信息

J Comp Neurol. 2006 Nov 20;499(3):471-84. doi: 10.1002/cne.21103.

DOI:10.1002/cne.21103
PMID:16998909
Abstract

Synaptopodin is an actin-associated molecule essential for the formation of a spine apparatus in telencephalic spines. To study whether synaptopodin and the spine apparatus organelle are regulated under conditions of lesion-induced plasticity, synaptopodin and the spine apparatus were analyzed in granule cells of the rat fascia dentata following entorhinal denervation. Confocal microscopy was employed to quantify layer-specific changes in synaptopodin-immunoreactive puncta densities. Electron microscopy was used to quantify layer-specific changes in spine apparatus organelles. Within the denervated middle and outer molecular layers, the layers of deafferentation-induced spine loss, synaptogenesis, and spinogenesis, the density of synaptopodin puncta and the number of spine apparatuses decreased by 4 days postlesion and slowly recovered in parallel with spinogenesis by 180 days postlesion. Within the nondenervated inner molecular layer, the zone without deafferentation-induced spine loss, a rapid loss of synaptopodin puncta and spine apparatuses was also observed. In this layer, spine apparatus densities recovered by 14 days postlesion, in parallel with plastic remodeling at the synaptic level and the postlesional recovery of granule cell activity. These data demonstrate layer-specific changes in the distribution of synaptopodin and the spine apparatus organelle following partial denervation of granule cells: in the layer of spine loss, spine apparatus densities follow spine densities; in the layer of spine maintenance, however, spine apparatus densities appear to be regulated by other signals.

摘要

突触素是一种与肌动蛋白相关的分子,对端脑棘中棘器的形成至关重要。为了研究突触素和棘器细胞器在损伤诱导可塑性条件下是否受到调控,在大鼠海马齿状回颗粒细胞中,对突触素和棘器进行了分析,这些颗粒细胞来自内嗅神经切断术后的大鼠。采用共聚焦显微镜对突触素免疫反应性小点密度的层特异性变化进行定量分析。利用电子显微镜对棘器细胞器的层特异性变化进行定量分析。在去神经支配的中分子层和外分子层,即去传入诱导的棘丢失、突触形成和棘生成的层中,突触素小点密度和棘器数量在损伤后4天减少,并在损伤后180天与棘生成平行缓慢恢复。在未去神经支配的内分子层,即无去传入诱导棘丢失的区域,也观察到突触素小点和棘器的快速丢失。在该层中,棘器密度在损伤后14天恢复,与突触水平的可塑性重塑和颗粒细胞活性的损伤后恢复平行。这些数据表明,颗粒细胞部分去神经支配后,突触素和棘器细胞器的分布存在层特异性变化:在棘丢失层,棘器密度随棘密度变化;然而,在棘维持层,棘器密度似乎受其他信号调控。

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