ACUTE AND LONG-TERM NEURONAL DEFICITS IN THE RAT OLFACTORY-BULB FOLLOWING ALCOHOL EXPOSURE DURING THE BRAIN GROWTH SPURT
ACUTE AND LONG-TERM NEURONAL DEFICITS IN THE RAT OLFACTORY-BULB FOLLOWING ALCOHOL EXPOSURE DURING THE BRAIN GROWTH SPURT
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DOI：
10.1016/0892-0362(91)90044-w
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发表时间：
1991-11-01
影响因子：
2.9
通讯作者：
WEST, JR
中科院分区：
文献类型：
--
作者：
BONTHIUS, DJ;WEST, JR
这项研究表明，在最初的酒精引起的缺陷后，嗅球颗粒细胞的数量相对恢复，而二尖瓣细胞的数量仍然永久且严重抑制。还证明了暴露模式对影响酒精引起的嗅球神经元损失严重程度的重要性。 Sprague-Dawley 幼鼠是人工饲养的，并在出生后第 4 天到第 9 天（PD）期间饮酒，这是大脑快速生长的时期，与人类妊娠晚期的部分时间相当。两组每天接受 4.5 g/kg 的酒精剂量，以 5.1% 或 10.2% 的溶液形式给药。第三组接受更高的每日酒精剂量，即 6.6 g/kg，以 2.5% 的溶液形式连续给药。幼崽要么在PD 10时被处死，要么被允许生长到成年并在PD 90时被处死。二尖瓣细胞和颗粒细胞的数量以及室管膜下区的面积由单个切片确定。在PD 10时，在酒精暴露后立即，在接受浓缩（5.1%和10.2%）酒精治疗的两组中，相对于对照组，二尖瓣细胞和颗粒细胞的数量均显着减少。然而，在PD 90时，接受浓缩溶液的组中只有二尖瓣细胞数量仍然显着减少，而颗粒细胞数量与对照组不再有显着差异。接受连续分次较高日剂量（6.6 g/kg）的组在 10 日或 90 日龄时没有明显的细胞损失。任何治疗或任何年龄对室管膜下区面积均无显着影响。这些结果表明，酒精对神经元数量的急性和长期影响因神经元群体而异，并且停止酒精暴露后某些神经元补体可能会发生代偿性变化。
This study demonstrates that there is a relative recovery in the number of olfactory bulb granule cells following an initial alcohol-induced deficit, while the number of mitral cells remains permanently and severely depressed. The importance of pattern of exposure in influencing the severity of alcohol-induced neuronal loss in the olfactory bulb is also demonstrated. Sprague-Dawley rat pups were reared artifically and were administered alcohol over postnatal days (PD) 4 through 9, a period of rapid brain growth comparable to part of the human third trimester. Two groups received a daily alcohol dose of 4.5 g/kg, administered either as a 5.1% or 10.2% solution. A third group received a higher daily alcohol dose of 6.6 g/kg administered continuously as a 2.5% solution. Pups were either sacrificed on PD 10 or were allowed to grow to adulthood and sacrificed on PD 90. The number of mitral cells and granule cells and the area of the subependymal zone were determined from single sections. On PD 10, immediately following the alcohol exposure, both the mitral cells and the granule cells were significantly reduced in number, relative to controls, in both of the groups receiving the concentrated (5.1% and 10.2%) alcohol treatments. On PD 90, however, only the mitral cell number remained significantly reduced in the groups receiving the concentrated solutions, while the number of granule cells no longer differed significantly from that of controls. The group receiving the higher daily dose (6.6 g/kg) in continuous fractions had no significant cell loss at 10 or 90 days of age. There was no significant effect of any treatment or at any age on the area of the subependymal zone. These results suggest that the acute and long-term effects of alcohol on neuronal number vary among neuronal populations and that compensatory changes may occur in some neuronal complements following cessation of the alcohol exposure.