Analyses of smooth endoplasmic reticulum of cerebellar parallel fibers in aging, ethanol-fed rats.
Analyses of smooth endoplasmic reticulum of cerebellar parallel fibers in aging, ethanol-fed rats.
复制标题
老年乙醇喂养大鼠小脑平行纤维平滑内质网的分析。
DOI：
10.1016/j.alcohol.2004.12.002
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Dlugos,CynthiaA
中科院分区：
文献类型：
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作者：
Dlugos,CynthiaA
滑面内质网（SER）是一种钙储存细胞器，对正常神经功能至关重要。SER的扩张是病理性的，并且对神经元钙稳态构成威胁。据报道，老年大鼠小脑浦肯野神经元树突内的SER扩张后，长期乙醇处理。乙醇相关的改变平行纤维SER尚未调查，尽管事实上，这种扩张可能先于并有助于跨突触SER扩张和变性浦肯野神经元树突。将雄性Fischer 344大鼠（n=120;年龄=12月龄）随机分为三个饮食组（每组40只大鼠），并喂食大鼠饲料、AIN-93 M液体对照饮食或AIN-93 M液体乙醇饮食（不含水）5、10、20或40周（每个时间点30只大鼠）。电镜观察后蚓小叶切片。测量了平行光纤SER分布的最大和最小直径。治疗5、10、20或40周后，未发现乙醇相关的平行纤维SER扩张。平行纤维SER分布确实发生了与纤维相关的扩张。这些发现支持以下观点：（1）平行纤维SER与浦肯野神经元的SER不同，对乙醇不敏感;（2）乙醇和衰老改变小脑功能和结构的机制不同。
The smooth endoplasmic reticulum (SER), a calcium storage organelle, is essential for normal neuronal function. Dilation of the SER is pathologic and a threat to neuronal calcium homeostasis. Dilation of the SER has been reported within the dendrites of cerebellar Purkinje neurons of aging rats after lengthy ethanol treatment. Ethanol-related alterations of parallel fiber SER have not been investigated despite the fact that such dilation may precede and contribute transsynaptically to SER dilation and degeneration in Purkinje neuron dendrites. Male Fischer 344 rats (n=120; age=12 months old) were randomly divided into three dietary groups (40 rats per group) and fed rat chow, the AIN-93M liquid control diet, or the AIN-93M liquid ethanol diet (without water) for 5, 10, 20, or 40 weeks (30 rats per time point). Sections from posterior vermal lobules were viewed with the electron microscope. Maximum and minimum diameters of parallel fiber SER profiles were measured. Ethanol-related dilation of parallel fiber SER was not found after 5, 10, 20, or 40 weeks of treatment. Age-related dilation of parallel fiber SER profiles did occur. These findings support the suggestions that (1) parallel fiber SER, unlike the SER in Purkinje neurons, is insensitive to ethanol and (2) the mechanisms by which ethanol and aging alter cerebellar function and structure are different.