Pentney R J, Quackenbush L J
Department of Anatomical Sciences, State University of New York, Buffalo 14214.
Alcohol Clin Exp Res. 1990 Dec;14(6):878-86. doi: 10.1111/j.1530-0277.1990.tb01831.x.
Metric parameters of Purkinje cell dendritic networks in 24- to 26-month-old Fischer 344 rats were determined after 48 weeks of chronic ethanol intake. Measurements included the total number and length of all segments/network, the total number and length of segments within topologically defined segment categories, and the mean length of segments in each category. A main effect of ethanol was expressed as a significant increase in cumulative length within one category of terminal segments. This increase was the result of a significant increase in mean length/segment in that category. Metric changes in other segment categories were not significant, showing that changes in the networks during ethanol treatment were not distributed randomly. Recovery after ethanol treatment was associated with further nonrandom remodeling of these networks. Significant differences in lengths of terminal segments were no longer present, but internal segments in networks of both pair-fed and ethanol-fed rats were significantly longer. Only one category of internal segments showed this change during recovery. The data showed that long term ethanol treatment in old rats, at a time when effects of aging processes were prominent in Purkinje cell networks, was associated with remodeling of those networks through dendritic extension. This effect was interpreted as compensatory growth in surviving networks following ethanol-related neuronal loss and/or damage to the surrounding neuropil. Recovery from dietary treatment produced further internal remodeling of those networks that was not related specifically to ethanol. It could be shown, however, that the restructuring processes that resulted in longer internal segments after dietary recovery were different in the pair-fed and the ethanolfed rats.
在对24至26月龄的Fischer 344大鼠进行48周的慢性乙醇摄入后，测定了浦肯野细胞树突网络的度量参数。测量内容包括所有节段/网络的总数和长度、拓扑定义的节段类别内节段的总数和长度，以及每个类别中节段的平均长度。乙醇的主要作用表现为某一类终末节段的累积长度显著增加。这种增加是该类别中节段平均长度显著增加的结果。其他节段类别的度量变化不显著，表明乙醇处理期间网络的变化并非随机分布。乙醇处理后的恢复与这些网络的进一步非随机重塑有关。终末节段长度的显著差异不再存在，但配对喂养和乙醇喂养大鼠网络中的内部节段显著更长。在恢复过程中，只有一类内部节段出现了这种变化。数据表明，在衰老过程对浦肯野细胞网络影响显著的老年大鼠中，长期乙醇处理与通过树突延伸对这些网络进行重塑有关。这种效应被解释为乙醇相关的神经元丢失和/或周围神经纤维网损伤后存活网络的代偿性生长。饮食处理后的恢复导致这些网络进一步的内部重塑，这与乙醇并无特异性关联。然而，可以证明，饮食恢复后导致内部节段变长的重组过程在配对喂养和乙醇喂养的大鼠中是不同的。
