Gu X Q, van der Kloot W
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794-8661.
Neuroscience. 1992;47(3):649-56. doi: 10.1016/0306-4522(92)90173-y.
This work was initiated because pretreatment with concanavalin A was reported to abolish the increase in spontaneous quantal release produced by hypertonic solutions [Gorio A. and Mauro A. (1979) J. gen. Physiol. 73, 245-263]. This suggested that lectins might be valuable tools for investigating the role of glycoproteins in the response to tonicity. We compared muscles soaked for 2 h in hypertonic solution containing concanavalin A with paired muscles soaked in hypertonic solution without lectin. The lectin treatment decreased miniature end-plate potential frequencies in Ringer and in hypertonic solutions compared with the controls. Even after lectin treatment hypertonic solutions and elevated K+ solutions increased miniature end-plate potential frequencies, and the proportional increases were the same as in controls. The lectin treatment lowered baseline frequency, but the preparation still responded to hypertonic solutions. Concanavalin A effects appeared after treatment for more than 1 h and required concentrations of 10 micrograms/ml or higher. Higher concentrations did not produce more effect. Similar results were obtained with four other lectins with different sugar specificities. Treatment in hypertonic solution without lectin produces a similar, but smaller, decrease in baseline frequency. Concanavalin A pretreatment had no detectable effects on evoked release or facilitation. We conclude that the effects of lectins on quantal release are not mediated by binding to a single sugar group. The lectins do not produce a unique effect; they exaggerate the changes produced by hypertonic pretreatment. All of the effects could be accounted for by a reduction in baseline [Ca2+] in the nerve terminal. Such reductions are produced by lectins in many cell types.
开展这项研究是因为有报道称，用伴刀豆球蛋白A进行预处理可消除高渗溶液引起的自发量子释放增加现象[戈里奥A.和毛罗A.（1979年）《普通生理学杂志》73卷，245 - 263页]。这表明凝集素可能是研究糖蛋白在对张力反应中作用的有价值工具。我们将在含伴刀豆球蛋白A的高渗溶液中浸泡2小时的肌肉与在不含凝集素的高渗溶液中浸泡的配对肌肉进行了比较。与对照组相比，凝集素处理降低了任氏液和高渗溶液中的微小终板电位频率。即使经过凝集素处理，高渗溶液和高钾溶液仍会增加微小终板电位频率，且增加的比例与对照组相同。凝集素处理降低了基线频率，但标本仍对高渗溶液有反应。伴刀豆球蛋白A的作用在处理1小时以上后出现，所需浓度为10微克/毫升或更高。更高浓度不会产生更大的效果。用其他四种具有不同糖特异性的凝集素也得到了类似结果。在不含凝集素的高渗溶液中处理会使基线频率产生类似但较小的降低。伴刀豆球蛋白A预处理对诱发释放或易化作用没有可检测到的影响。我们得出结论，凝集素对量子释放的作用不是通过与单个糖基团结合介导的。凝集素不会产生独特的作用；它们会夸大高渗预处理产生的变化。所有这些作用都可以用神经末梢基线[Ca2+]的降低来解释。许多细胞类型中的凝集素都会产生这种降低。
