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在脑发育激增期,单日饮酒会导致脑重量受限以及小脑浦肯野细胞丢失。

A single day of alcohol exposure during the brain growth spurt induces brain weight restriction and cerebellar Purkinje cell loss.

作者信息

Goodlett C R, Marcussen B L, West J R

机构信息

Department of Anatomy, University of Iowa College of Medicine, Iowa City 52242.

出版信息

Alcohol. 1990 Mar-Apr;7(2):107-14. doi: 10.1016/0741-8329(90)90070-s.

Abstract

The period of rapid brain growth that occurs relatively late in development has been shown to be vulnerable to alcohol-induced brain growth deficits and neuron loss in rats using repeated daily exposure to alcohol. This study examined whether a condensed exposure (binge) restricted to a single day during this period would be sufficient to restrict brain growth and produce neuron depletion. Using artificial rearing, alcohol was given to neonatal rats in two consecutive feedings on postnatal day 4, using a total dose of either 6.6 g/kg or 3.3 g/kg. The higher dose produced mean peak blood alcohol concentrations of 362 mg/dl, while the lower dose produced mean peak BACs of 153 mg/dl. The higher dose significantly restricted whole brain, forebrain, cerebellum and brain stem weights on postnatal day 10, with the cerebellum being most severely reduced. Cerebellar Purkinje cells, counted from a 2-microns section from the midsagittal vermis, were significantly reduced in the 6.6 g/kg group. Purkinje cell loss relative to controls was significant in the most lobules (I-V, IX and X), but, notably, was not significant in the later maturing regions (lobules VI and VII). The 3.3 g/kg group had no significant reductions in regional brain weights. Although the overall number of Purkinje cells was nonsignificantly reduced relative to controls, the 3.3 g/kg dose did produce significant loss of Purkinje cells in lobule II. Exposure to high peak BACs, even for a relatively short period during the brain growth spurt, constitutes a substantial risk to the developing brain, and even a moderate exposure may result in loss of more vulnerable neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在发育过程中相对较晚出现的脑快速生长阶段,已被证明易受酒精诱导的脑生长缺陷和神经元损失影响,这是通过对大鼠每日重复暴露于酒精得出的结论。本研究检测了在此期间仅一天的集中暴露(暴饮)是否足以限制脑生长并导致神经元减少。采用人工饲养方式,在出生后第4天对新生大鼠连续两次喂食酒精,总剂量分别为6.6 g/kg或3.3 g/kg。较高剂量产生的平均血酒精浓度峰值为362 mg/dl,而较低剂量产生的平均血酒精浓度峰值为153 mg/dl。较高剂量在出生后第10天显著限制了全脑、前脑、小脑和脑干的重量,其中小脑重量减少最为严重。从矢状中蚓部2微米切片中计数的小脑浦肯野细胞,在6.6 g/kg组中显著减少。相对于对照组,浦肯野细胞损失在大多数小叶(I-V、IX和X)中显著,但值得注意的是,在较晚成熟的区域(小叶VI和VII)中并不显著。3.3 g/kg组的区域脑重量没有显著减少。虽然相对于对照组,浦肯野细胞的总数减少不显著,但3.3 g/kg剂量确实在小叶II中导致了浦肯野细胞的显著损失。即使在脑生长突增期间相对较短的时间内暴露于高血酒精浓度峰值,也会对发育中的脑构成重大风险,甚至适度暴露也可能导致更易受损神经元的损失。(摘要截断于250字)

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