Dlugos Cynthia A
Department of Pathology and Anatomical Sciences, School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York 14214-3000, USA.
Alcohol Clin Exp Res. 2006 May;30(5):883-91. doi: 10.1111/j.1530-0277.2006.00103.x.
Long-term ethanol consumption in aging rats results in degeneration and regression of the Purkinje neuron (PN) dendritic arbor. One marked ethanol-related change in Purkinje dendrite ultrastructure is dilation of the smooth endoplasmic reticulum (SER) within PN dendritic shafts. The purpose of this study was to determine a time course for ethanol-related dendritic regression in PN dendritic shafts and spines.
One-hundred eighty aging, male Fischer 344 rats were used. Four durations of treatment (5, 10, 20, and 40 weeks) and 3 dietary treatment groups (60 rats/treatment group) were studied. Ethanol-fed rats received a liquid ethanol diet (35% of dietary calories from ethanol). Pair-fed rats received an isocaloric liquid control diet and chow-fed rats received rat chow and water ad libitum. After each duration of treatment, 45 rats (15/treatment) were euthanized and 2 posterior cerebellar lobules/rat were viewed with electron microscopy and photographed. Diameters of SER profiles within PN shafts and spines were measured with image analysis.
Ethanol-related SER dilation in dendritic shafts occurred following 40 weeks of treatment. Ethanol-related SER dilation was not detected in PN dendritic spines.
These results confirm that ethanol-related dilation of SER profiles in PN dendritic shafts occurs following the same duration of treatment as the dendritic regression previously reported in other studies. Degenerating bodies that may be linked to dendritic regression were also identified in PN dendrites.
衰老大鼠长期摄入乙醇会导致浦肯野神经元(PN)树突分支发生退化和萎缩。PN树突轴内滑面内质网(SER)扩张是与乙醇相关的浦肯野树突超微结构的一个显著变化。本研究的目的是确定PN树突轴和树突棘中与乙醇相关的树突萎缩的时间进程。
使用180只衰老雄性Fischer 344大鼠。研究了4个治疗时长(5、10、20和40周)和3个饮食治疗组(每组60只大鼠)。乙醇喂养的大鼠接受液体乙醇饮食(乙醇提供35%的饮食热量)。配对喂养的大鼠接受等热量液体对照饮食,正常饮食喂养的大鼠自由摄食大鼠饲料和水。每个治疗时长结束后,对45只大鼠(每组15只)实施安乐死,对每只大鼠的2个小脑后叶进行电子显微镜观察并拍照。通过图像分析测量PN轴和树突棘内SER轮廓的直径。
治疗40周后,树突轴出现与乙醇相关的SER扩张。在PN树突棘中未检测到与乙醇相关的SER扩张。
这些结果证实,PN树突轴中与乙醇相关的SER轮廓扩张发生的治疗时长与先前其他研究报道的树突萎缩时长相同。在PN树突中还发现了可能与树突萎缩有关的退化小体。