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单一延长应激诱导中缝背核内 CaM/CaMKIIα 的变化。

Single-prolonged stress induce changes of CaM/CaMKIIα in the rats of dorsal raphe nucleus.

机构信息

Department of Histology and Embryology, Institute of Pathology and Pathophysiology, Basic Medical Sciences College, China Medical University, 92 North 2nd Road, Shenyang 110001, Liaoning Province, People’s Republic of China.

出版信息

Neurochem Res. 2012 May;37(5):1043-9. doi: 10.1007/s11064-012-0705-5.

Abstract

Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) is identified as a Ca2+-dependent kinase in brain involved in the activation of Tryptophan hydroxylase (TPH) acting through direct phosphorylation of TPH, and playing key roles in the signaling pathways initiated by various G protein-coupled 5-HT receptors. The goal of this study is to detect whether there are changes of CaM and CaMKIIα in dorsal raphe nucleus in the rats exposed to single-prolonged stress (SPS), which is a model employed in post-traumatic stress disorder (PTSD) study extensively. A total of 90 male Wistar rats were randomly divided into a normal control group and SPS groups of 7d, 14d. The changes of CaM/CaMKIIα were detected by immunohistochemistry, reverse transcription-polymerase chain reaction and western blot. Our results demonstrate that both expressions of CaM and CaMKIIα significantly increase (P < 0.001) in the SPS 7d group than that in the control group, and then decreased dramatically (P < 0.001) 14 days after SPS. Our results confirm that SPS induce changes of CaM/CaMKIIα in the dorsal raphe nucleus. Changes of CaM/CaMKIIα may be associated with the activation of 5-HT1A receptor, and may contribute to the progress of molecular mechanism of PTSD.

摘要

钙/钙调蛋白依赖性蛋白激酶 IIα(CaMKIIα)是一种在大脑中被发现的钙依赖性激酶,它通过直接磷酸化色氨酸羟化酶(TPH)来激活 TPH,从而在各种 G 蛋白偶联 5-HT 受体引发的信号通路中发挥关键作用。本研究的目的是检测在单一延长应激(SPS)暴露的大鼠中,中缝背核中是否存在钙调蛋白和 CaMKIIα 的变化,SPS 是创伤后应激障碍(PTSD)研究中广泛采用的模型。90 只雄性 Wistar 大鼠随机分为正常对照组和 SPS 组(7d、14d)。通过免疫组织化学、逆转录聚合酶链反应和 Western blot 检测 CaM/CaMKIIα 的变化。我们的结果表明,SPS 7d 组中 CaM 和 CaMKIIα 的表达均显著增加(P < 0.001),而在 SPS 后 14 天则显著降低(P < 0.001)。我们的结果证实 SPS 诱导中缝背核中 CaM/CaMKIIα 的变化。CaM/CaMKIIα 的变化可能与 5-HT1A 受体的激活有关,并可能有助于 PTSD 分子机制的进展。

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