Pentney R J
Department of Anatomical Sciences, State University of New York, Buffalo 14214.
Alcohol Alcohol Suppl. 1991;1:393-7.
Chronic ethanol treatment and aging processes produce significant changes in neuronal dendritic morphometry, but the precise patterns of change are different for these two factors. Furthermore, the morphometric effects of long term ethanol treatment on neuronal structure may be expressed in different ways at different times during the life span. When rats were treated with ethanol chronically from 12 months of age for 24 or 48 weeks, the predominant morphometric change in surviving cerebellar Purkinje neurons was a nonrandom elongation of terminal segments in the dendritic arbors. The results suggested that the synaptic circuitry in the cerebellar cortex of these rats was altered in an ethanol-specific and nonrandom pattern by selective compensatory growth of a particular category of terminal segments. During normal aging between 12 and 18 months, Purkinje cell networks in rats underwent regression of terminal dendritic segments, but after 18 months localized regrowth of proximal terminal dendritic segments coincided with regression of distal terminal segments, a pattern of dendritic change that was markedly different from that induced by ethanol.
长期乙醇处理和衰老过程会使神经元树突形态发生显著变化，但这两个因素导致的具体变化模式有所不同。此外，长期乙醇处理对神经元结构的形态学影响可能在生命周期的不同时间以不同方式表现出来。当大鼠从12个月龄开始接受24周或48周的慢性乙醇处理时，存活的小脑浦肯野神经元中主要的形态学变化是树突分支中终末节段的非随机延长。结果表明，这些大鼠小脑皮质中的突触回路通过特定终末节段的选择性代偿性生长，以乙醇特异性和非随机模式发生改变。在12至18个月的正常衰老过程中，大鼠的浦肯野细胞网络经历了终末树突节段的退化，但18个月后，近端终末树突节段的局部再生与远端终末节段的退化同时发生，这种树突变化模式与乙醇诱导的模式明显不同。
