Surface exposure of synaptosomal gangliosides from long-sleep and short-sleep mice.

Surface exposure of synaptosomal gangliosides from long-sleep and short-sleep mice.
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DOI:
10.1111/j.1530-0277.1992.tb01882.x
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发表时间:
1992-10
期刊:
Alcoholism, clinical and experimental research
影响因子:
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通讯作者:
M. Ullman;R. F. Ventura;L. Draski;R. Deitrich;R. Baker
M. Ullman;R. F. Ventura;L. Draski;R. Deitrich;R. Baker
中科院分区:
其他
文献类型:
--
作者:
M. Ullman;R. F. Ventura;L. Draski;R. Deitrich;R. Baker

文献摘要

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用半乳糖氧化酶/NaB[~H]4技术检测了长睡眠(LS)和短睡眠(SS)小鼠全脑突触体内神经节苷脂的相对表面暴露。单唾液酸神经节苷脂GM1的表面暴露在两个品系之间没有差异。然而,在LS突触体内,多唾液酸神经节苷脂GD1a、GD1b和GT1b的表面暴露显著大于SS。神经氨酸酶在早期将多唾液酸神经节苷脂水解为最终产物GM1,在LS中比在SS突触体内发生得更快。250 mM或50 mM乙醇暴露后,LS突触体神经节苷脂表面暴露减少,而SS表面暴露增加。对各个神经节苷脂类别的配对比较表明,与对照组相比,LS突触体神经节苷脂表面暴露的减少可归因于多唾液酸神经节苷脂的减少。然而,乙醇诱导的SS突触体神经节苷脂表面暴露的增加主要是由于仅GD1a表面暴露的增加。这些结果表明,神经节苷脂表面暴露的内在差异和/或乙醇引起的神经节苷脂表面分布变化的幅度和方向的内在差异可能反映了这类化合物改变膜对乙醇敏感性的生物物理或调节机制。这些结果表明,应该进行进一步的研究,以确定神经节苷脂是否是遗传决定的乙醇敏感性的因素。
A galactose oxidase/NaB[3H]4 technique was used to examine the relative surface exposure of gangliosides from whole brain synaptosomes of long-sleep (LS) and short-sleep (SS) mice. The surface exposure of the monosialoganglioside, GM1, did not differ between the two lines. Surface exposure of the polysialogangliosides GD1a, GD1b, and GT1b, however, was significantly greater in LS synaptosomes than in SS. Hydrolysis of the polysialogangliosides by neuraminidase to the end-product, GM1, at early time periods occurred more rapidly in LS than in SS synaptosomes. Upon exposure to either 250 mM or 50 mM ethanol, LS synaptosomal ganglioside surface exposure was decreased, but that of SS was increased. Pairwise comparisons of the individual ganglioside classes indicated that the decrease in LS synaptosomal ganglioside surface exposure was attributable to decreases in the polysialogangliosides, compared with controls. The ethanol-induced increase in SS synaptosomal ganglioside surface exposure, however, was mainly due to an increased surface exposure of only GD1a. These results suggest that intrinsic differences in the surface exposure of gangliosides and/or the magnitude and direction of ethanol-induced changes in ganglioside surface distribution may reflect biophysical or modulatory mechanisms by which this class of compounds modifies membrane sensitivity to ethanol. These results suggest that further studies should be performed to determine whether gangliosides are factors in genetically determined sensitivity to ethanol.