Stress-induced phosphorylation of SNAP-25.
Stress-induced phosphorylation of SNAP-25.
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应激诱导的 SNAP-25 磷酸化。
DOI：
10.1016/j.neulet.2013.12.044
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Takahashi M
中科院分区：
文献类型：
--
作者：
Yamamori S;Sugaya D;Iida Y;Kokubo H;Itakura M;Suzuki E;Kataoka M;Miyaoka H;Takahashi M
突触体相关蛋白25 kDa（SNAP-25）是一种t-SNARE蛋白，在通过胞吐作用释放神经递质中起关键作用。蛋白激酶C使SNAP-25在Ser 187处磷酸化，然而这种磷酸化事件在脑功能中的生理意义仍不清楚。在本研究中，我们发现SNAP-25磷酸化在冷水束缚应激后小鼠脑中迅速增加。SNAP-25的基础和应激诱导的磷酸化在应激相关的大脑区域（包括大脑皮层、海马和杏仁核）中均较高，并且磷酸化的程度随着应激量的增加而增加。静脉注射肾上腺素增加SNAP-25磷酸化，尽管在肾上腺切除小鼠中仍然观察到应激诱导的磷酸化。这些结果表明，SNAP-25磷酸化是通过中枢和外周机制以应激依赖性方式调节的。
Synaptosomal-associated protein of 25 kDa (SNAP-25), a t-SNARE protein, plays a crucial role in neurotransmitter release by exocytosis. Protein kinase C phosphorylates SNAP-25 at Ser187, however the physiological significance of this phosphorylation event in brain function remains unclear. In the present study, we found that SNAP-25 phosphorylation increased rapidly in the mouse brain following cold-water restraint stress. Both basal and stress-induced phosphorylation of SNAP-25 were high in stress-related brain regions, including the cerebral cortex, hippocampus, and amygdala, and the extent of phosphorylation increased with increasing amounts of stress. Intravenous administration of adrenaline increased SNAP-25 phosphorylation, although stress-induced phosphorylation was still observed in adrenalectomized mice. These results indicate that SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms.