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咀嚼可增强应激诱导的大鼠扣带回皮质中 pERK-免疫反应细胞的增加。

Chewing augments stress-induced increase of pERK-immunoreactive cells in the rat cingulate cortex.

机构信息

Orthodontic Division, Department of Oral Science, Graduate School of Dentistry, Kanagawa Dental University, Inaoka-Cho 82, Yokosuka, Kanagawa, 238-8580, Japan.

Department of Oral Surgery, Jichi Medical University Hospital, Yakushiji, 3311-1, Shimotsuke, Tochigi, 329-0498, Japan.

出版信息

Neurosci Lett. 2020 May 14;727:134921. doi: 10.1016/j.neulet.2020.134921. Epub 2020 Mar 19.

DOI:10.1016/j.neulet.2020.134921
PMID:32201242
Abstract

The eff ;ects of chewing during restraint stress on the anterior, mid- and posterior cingulate cortices were investigated in rats using immunohistochemistry to detect the expression of phosphorylated extracellular signal-regulated kinase 1 and 2 (pERK1/2), a marker of responding cells. The rats were divided into three groups: control (no immobilization), stress-only (immobilized), and stress-with-chewing (immobilized and allowed to chew a wooden stick). Significant increases in the number of pERK1/2-immunoreactive cells in the anterior, mid- and posterior cingulate cortices were noted in the stress-only group when compared with the control group (p < 0.05). Furthermore, the number of pERK1/2-immunoreactive cells in the anterior, mid- and posterior cingulate cortices in the stress-with-chewing group was also significantly higher than that in the stress-only group (p < 0.05). These findings indicate that the cingulate cortex plays a role in the negative-feedback effect and might be an essential part of the brain where the ameliorating effects of chewing against stress are produced.

摘要

使用免疫组织化学方法检测磷酸化细胞外信号调节激酶 1 和 2(pERK1/2)的表达,来研究束缚应激时咀嚼对大鼠前扣带回皮质、中扣带回皮质和后扣带回皮质的影响,pERK1/2 是反应细胞的标志物。将大鼠分为三组:对照组(无固定)、应激组(固定)和应激加咀嚼组(固定并允许咀嚼木棍)。与对照组相比,应激组大鼠前扣带回皮质、中扣带回皮质和后扣带回皮质中 pERK1/2 免疫反应细胞的数量明显增加(p<0.05)。此外,应激加咀嚼组大鼠前扣带回皮质、中扣带回皮质和后扣带回皮质中 pERK1/2 免疫反应细胞的数量也明显高于应激组(p<0.05)。这些发现表明扣带回皮质在负反馈效应中起作用,可能是咀嚼对抗应激的缓解作用产生的大脑的重要组成部分。

相似文献

1
Chewing augments stress-induced increase of pERK-immunoreactive cells in the rat cingulate cortex.咀嚼可增强应激诱导的大鼠扣带回皮质中 pERK-免疫反应细胞的增加。
Neurosci Lett. 2020 May 14;727:134921. doi: 10.1016/j.neulet.2020.134921. Epub 2020 Mar 19.
2
Chewing ameliorates the effects of restraint stress on pERK-immunoreactive neurons in the rat insular cortex.咀嚼可改善束缚应激对大鼠岛叶皮质中pERK免疫反应性神经元的影响。
Neurosci Lett. 2018 May 1;674:60-65. doi: 10.1016/j.neulet.2018.03.008. Epub 2018 Mar 6.
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Chewing suppresses the stress-induced increase in the number of pERK-immunoreactive cells in the periaqueductal grey.咀嚼可抑制应激诱导的中脑导水管周围灰质中pERK免疫反应性细胞数量的增加。
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Combination of chewing and stress up-regulates hippocampal glucocorticoid receptor in contrast to the increase of mineralocorticoid receptor under stress only.咀嚼和压力的结合会使海马体的糖皮质激素受体上调,而仅在压力下会增加盐皮质激素受体。
Neurosci Lett. 2012 Jun 21;519(1):20-5. doi: 10.1016/j.neulet.2012.04.080. Epub 2012 May 8.
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Chewing reduces sympathetic nervous response to stress and prevents poststress arrhythmias in rats.咀嚼可降低大鼠对应激的交感神经反应,并预防应激后心律失常。
Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1551-8. doi: 10.1152/ajpheart.01224.2010. Epub 2011 Aug 5.
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Chewing rescues stress-suppressed hippocampal long-term potentiation via activation of histamine H1 receptor.咀嚼通过激活组胺H1受体挽救应激抑制的海马长时程增强。
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Chewing ameliorates stress-induced suppression of spatial memory by increasing glucocorticoid receptor expression in the hippocampus.咀嚼通过增加海马中的糖皮质激素受体表达来改善应激引起的空间记忆抑制。
Brain Res. 2012 Mar 29;1446:34-9. doi: 10.1016/j.brainres.2012.01.011. Epub 2012 Jan 16.
8
Chewing ameliorates stress-induced suppression of hippocampal long-term potentiation.咀嚼可改善应激诱导的海马体长期增强抑制。
Neuroscience. 2008 Jul 17;154(4):1352-9. doi: 10.1016/j.neuroscience.2008.04.057. Epub 2008 May 3.
9
Short-term anesthesia inhibits formalin-induced extracellular signal-regulated kinase (ERK) activation in the rostral anterior cingulate cortex but not in the spinal cord.短期麻醉可抑制福尔马林诱导的前额叶前扣带回皮质细胞外信号调节激酶(ERK)的激活,但对脊髓无此作用。
Mol Pain. 2015 Aug 14;11:49. doi: 10.1186/s12990-015-0052-z.
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Suppression of stress immobilization-induced phosphorylation of ERK 1/2 by biting in the rat hypothalamic paraventricular nucleus.
Neurosci Lett. 2005;383(1-2):160-4. doi: 10.1016/j.neulet.2005.04.011.

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