Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus
Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus
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DOI：
10.1016/j.neulet.2005.04.011
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发表时间：
2005-07
影响因子：
2.5
通讯作者：
K. Sasaguri;M. Kikuchi;N. Hori;N. Yuyama;M. Onozuka;S. Sato
中科院分区：
文献类型：
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作者：
K. Sasaguri;M. Kikuchi;N. Hori;N. Yuyama;M. Onozuka;S. Sato
我们之前曾报道过急性固定应激会诱导 Fos 蛋白的产生。 Fos 蛋白通常用作神经元活动的标记物，并且与下丘脑室旁核 (PVN) 中细胞外信号调节蛋白激酶 1/2 (pERK1/2) 的磷酸化有关。应激期间的咬行为降低了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会诱导 PVN 中的 pERK1/2，以及应激诱导的 pERK1/2 是否会因同时咬合行为而减弱。急性固定应激（增量最多 15 分钟）会产生可检测量的 pERK1/2，其量与应激间隔时间成正比。急性固定应激期间的咬合显着降低了可检测到的 pERK1/2 的量。这些结果表明，急性应激期间的咬合活动会抑制大脑该区域的 pERK1/2。神经元细胞对急性应激的反应在某种程度上可能是通过咬合抑制 pERK1/2 来调节的。
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.