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大鼠海马注射红藻氨酸损伤后CA1区锥体细胞去神经支配诱导的树突改变

Denervation-induced dendritic alterations in CA1 pyramidal cells following kainic acid hippocampal lesions in rats.

作者信息

Pyapali G K, Turner D A

机构信息

Department of Surgery [Neurosurgery], Duke University Medical Center, Durham, NC 27710.

出版信息

Brain Res. 1994 Aug 1;652(2):279-90. doi: 10.1016/0006-8993(94)90238-0.

Abstract

Kainic acid (KA) lesions of the CA3 region of the hippocampus lead to denervation of ipsilateral CA1 neurons. To assess denervation-induced post-synaptic changes, intracellular physiological recordings were performed in the CA1 region in vitro, from both control and KA-treated tissue. The neurons were intracellularly stained with neurobiotin, reconstructed using a quantitative three-dimensional system and analyzed for morphometric and electrotonic parameters. Total dendritic length was slightly longer in the denervated CA1 cells and there was a selective and significant increase in both branches and terminals in the mid-stratum radiatum (300-550 microns from the soma using Sholl analysis) in the KA-treated rats compared to untreated controls, particularly for cells at 5 days post-lesion and later, which exhibited graded synaptically-evoked bursts. However, there was no significant difference in the basal dendritic arborization. Electrotonic modelling of the dendritic structure revealed specific membrane resistivity values of 33.4 k omega.cm2 for the normal CA1 cells and 29.8 K omega-cm2 for the KA-treated cells, assuming an internal resistivity of 200 omega.cm2, shrinkage correction of 1.57 and a spatial distribution of dendritic spines. The number of dendritic terminals of these denervated CA1 neurons at electrotonic distances between 0.5 lambda and 0.7 lambda also significantly increased in the cells from KA-treated animals. These findings indicate that there is a selective and specific increase in the number of apical terminals and dendritic branches following the unilateral kainic acid lesion. These apical branch changes may represent dendritic sprouting as a post-synaptic response to the denervation, which was particularly marked in neurons exhibiting graded synaptic bursting behavior.

摘要

海马体CA3区的海藻酸(KA)损伤会导致同侧CA1神经元去神经支配。为了评估去神经支配引起的突触后变化,在体外对对照组和KA处理组的CA1区组织进行了细胞内生理记录。用神经生物素对神经元进行细胞内染色,使用定量三维系统进行重建,并分析形态学和电紧张参数。去神经支配的CA1细胞的总树突长度略长,与未处理的对照组相比,KA处理的大鼠在辐射层中部(使用肖尔分析,距胞体300 - 550微米)的分支和终末有选择性且显著增加,特别是在损伤后5天及以后的细胞,这些细胞表现出分级的突触诱发爆发。然而,基底树突分支没有显著差异。对树突结构进行电紧张建模,假设内部电阻率为200Ω.cm2、收缩校正为1.57以及树突棘的空间分布,正常CA1细胞的特定膜电阻率值为33.4kΩ.cm2,KA处理的细胞为29.8kΩ.cm2。在KA处理动物的细胞中,这些去神经支配的CA1神经元在电紧张距离0.5λ至0.7λ之间的树突终末数量也显著增加。这些发现表明,单侧海藻酸损伤后,顶端终末和树突分支的数量有选择性和特异性增加。这些顶端分支变化可能代表树突发芽,作为对去神经支配的突触后反应,在表现出分级突触爆发行为的神经元中尤为明显。

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