Moretto M B, de Mattos-Dutra A, Arteni N, Meirelles R, de Freitas M S, Netto C A, Pessoa-Pureur R
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Neurochem Res. 1999 Oct;24(10):1263-9. doi: 10.1023/a:1020925107130.
Synapsins are phosphoproteins related to the anchorage of synaptic vesicles to the actin skeleton. Hypoxia-ischemia causes an increased calcium influx into neurons through ionic channels gated by activation of glutamate receptors. In this work seven-day-old Wistar rats were submitted to hypoxia-ischemia and sacrificed after 21 hours, 7, 30, or 90 days. Synaptosomal fractions were obtained by Percoll gradients and incubated with 32P (10 microCi/g). Proteins were analysed by SDS-PAGE and radioactivity incorporated into synapsin 1 was counted by liquid scintillation. Twenty-one hours after hypoxia-ischemia we observed a reduction on the in vitro phosphorylation of synapsin 1, mainly due to hypoxia, rather than to ischemia; this effect was reversed at day 7 after the insult. There was another decrease in phosphorylation 30 days after the event interpreted as a late effect of hypoxia-ischemia. No changes were observed at day 90. Our results suggest that decreased phosphorylation of synapsin 1 could be related to neuronal death that follows hypoxia-ischemia.
突触素是与突触小泡锚定到肌动蛋白骨架相关的磷蛋白。缺氧缺血会导致通过谷氨酸受体激活门控的离子通道使钙离子流入神经元增加。在这项研究中，将7日龄的Wistar大鼠进行缺氧缺血处理，并在21小时、7天、30天或90天后处死。通过Percoll梯度获得突触体组分，并与32P（10微居里/克）一起孵育。通过SDS-PAGE分析蛋白质，并通过液体闪烁计数掺入突触素1中的放射性。缺氧缺血21小时后，我们观察到突触素1的体外磷酸化减少，主要是由于缺氧，而非缺血；这种效应在损伤后第7天逆转。事件发生30天后磷酸化再次降低，这被解释为缺氧缺血的晚期效应。在第90天未观察到变化。我们的结果表明，突触素1磷酸化降低可能与缺氧缺血后的神经元死亡有关。
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