首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus.
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Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus.

机译:咬住大鼠下丘脑室旁核,抑制应激固定诱导的ERK 1/2磷酸化。

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摘要

We have previously reported that acute immobilization stress induces Fos protein. Fos protein is generally used as a marker for neuronal activity and has been linked to phosphorylation of extracellular signal-regulated protein kinase 1/2 (pERK1/2), in the hypothalamic paraventricular nucleus (PVN). Biting behavior during the period of stress reduced the expression of Fos protein. The present immunohistochemical study was designed to determine whether acute immobilization stress induces pERK1/2 in the PVN, and whether the stress-induced pERK1/2 was attenuated by simultaneous biting behavior. Acute immobilization stress, in increments of up to 15min, produced detectable amounts of pERK1/2 that were proportional to the interval of stress. Biting during the acute immobilization stress significantly reduced the amount of detectable pERK1/2. These results suggest that biting activity during acute stress inhibits pERK1/2 in this region of the brain. It is feasible that the neuronal cellular response to acute stress is regulated, in some part, by inhibition of pERK1/2 by biting.
机译:我们以前曾报道过,急性固定应激会诱导Fos蛋白。 Fos蛋白通常用作神经元活动的标记,并已与下丘脑室旁核(PVN)中细胞外信号调节的蛋白激酶1/2(pERK1 / 2)的磷酸化有关。应激期间的咬人行为降低了Fos蛋白的表达。本免疫组织化学研究旨在确定急性固定应激是否在PVN中诱导pERK1 / 2,以及同时诱导的咬咬行为是否减弱了应激诱导的pERK1 / 2。急性固定应激以最多15分钟的增量产生可检测到的pERK1 / 2量,该量与应激间隔成正比。急性固定压力期间的咬伤显着减少了可检测的pERK1 / 2的量。这些结果表明,急性应激时的咬人活动会抑制大脑此区域的pERK1 / 2。通过咬咬抑制pERK1 / 2来调节对急性应激的神经元细胞反应是可行的。

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