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神经节苷脂抗体增强脑片去极化诱导的γ-氨基丁酸释放

Enhancement of depolarization-induced release of gamma-aminobutyric acid from brain slices by antibodies to ganglioside.

作者信息

Frieder B, Rapport M M

出版信息

J Neurochem. 1981 Sep;37(3):634-9. doi: 10.1111/j.1471-4159.1982.tb12534.x.

Abstract

The effect of antibodies to GM1 ganglioside on release of neurotransmitters from rat brain slices was studied. Depolarization-induced (40 mM-KCl or veratrine) release of gamma-aminobutyric acid was markedly enhanced. Depolarization-induced release of norepinephrine was only slightly enhanced, whereas that of serotonin was unaffected. No effect on spontaneous release was observed for any of these three neurotransmitters. These results show that antibodies that can bind to synaptic membrane antigens may alter neurotransmitter release and that antibodies directed against GM1 ganglioside exhibit a measure of specificity in producing such an effect.

摘要

研究了抗GM1神经节苷脂抗体对大鼠脑片神经递质释放的影响。去极化诱导(40 mM - 氯化钾或藜芦碱)的γ-氨基丁酸释放显著增强。去极化诱导的去甲肾上腺素释放仅略有增强,而5-羟色胺的释放则不受影响。对于这三种神经递质中的任何一种,均未观察到对自发释放的影响。这些结果表明,能够与突触膜抗原结合的抗体可能会改变神经递质的释放,并且针对GM1神经节苷脂的抗体在产生这种效应时表现出一定程度的特异性。

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