Pentney R J
Department of Anatomical Sciences, School of Medicine and Biomedical Sciences, State University of New York at Buffalo 14214-3000, USA.
Alcohol Alcohol. 1995 Jan;30(1):87-96.
The present study proposed to determine the significance of previously reported ethanol-induced dendritic lengthening in mature cerebellar Purkinje neurons (PN). An analysis of dendritic path lengths (PL) was used to make this determination. A PL is the curvilinear length from the origin of the dendritic root segment to the free tip of a dendritic terminal. It was hypothesized that treatment-induced dendritic lengthening resulted from dendritic growth, and that growth should produce an upward shift in the value of the median PL. The PL and the segment length (SL) for each dendritic terminal were measured in PN of 24 month old male F344 rats, previously fed a liquid diet containing 35% ethanol-derived calories for 48 weeks, to test that hypothesis. Because there are large numbers of terminal dendrites in PN networks a shift in the value of their median PL is a sensitive measure of change in these networks. It was found that almost 30% of the ethanol-exposed cell sample had median PL that were shorter than expected and that the median SL in these same neurons tended to be longer than expected. At the end of the ethanol treatment, half of these rats were weaned from the ethanol diet for a subsequent 8 weeks to test for reversibility of these changes. Following the period of abstinence from dietary ethanol, the significant ethanol-related differences previously found in dendritic lengths were no longer present. A consideration of two models of dendritic regression suggested that elongation of surviving terminal dendritic segments in the ethanol-exposed neurons occurred through deletion of other terminal segments at their vertices (branch points). It was shown that deletions of entire terminal dendritic segments at their vertices would produce increases in the lengths of associated terminal segments in the absence of real growth. Deletions of dendritic segments would also entail loss of PL unique to the deleted segments, thereby causing a shift in the value of the median PL of affected networks.
本研究旨在确定先前报道的乙醇诱导成熟小脑浦肯野神经元（PN）树突延长的意义。通过分析树突路径长度（PL）来进行这一测定。PL是从树突根部段的起点到树突末端自由尖端的曲线长度。据推测，治疗诱导的树突延长是由树突生长引起的，并且这种生长应导致中位PL值向上偏移。在24月龄雄性F344大鼠的PN中测量每个树突末端的PL和段长度（SL），这些大鼠先前喂食含35%乙醇热量的液体饮食48周，以检验该假设。由于PN网络中有大量的终末树突，它们中位PL值的变化是这些网络变化的敏感指标。结果发现，近30%的乙醇暴露细胞样本的中位PL比预期短，并且这些相同神经元的中位SL往往比预期长。在乙醇治疗结束时，将这些大鼠中的一半从乙醇饮食中断奶8周，以测试这些变化的可逆性。在戒断饮食乙醇一段时间后，先前在树突长度上发现的与乙醇相关的显著差异不再存在。对两种树突消退模型的考虑表明，乙醇暴露神经元中存活的终末树突段的延长是通过在其顶点（分支点）删除其他终末段而发生的。结果表明，在没有实际生长的情况下，在其顶点删除整个终末树突段会导致相关终末段长度增加。树突段的删除也将导致被删除段特有的PL损失，从而导致受影响网络的中位PL值发生偏移。
