The Expression of Neurodegeneration-Related Genes in the Hippocampus of Hypothyroid Rats Following Long-Term Potentiation.

IF 0.9 Q3 MEDICINE, GENERAL & INTERNAL
Melek Altunkaya, Ercan Babur, Özlem Barutçu, Cem Süer, Nurcan Dursun
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引用次数: 0

Abstract

Background:  In our research, we examined how the induction of long-term potentiation (LTP) in the hippocampus of hypothyroid rats afects the mRNA levels of several proteins involved with neurodegeneration, including Gsk3, Cdk5, Akt1, Mapt, P35 (Anxa), Capn1, Bace1, and Psen2.

Methods:  Wistar-albino rats, consisting of 12 males, were used in the research, and they were separated into 2 groups: control (n=6) and hypothyroidism (n=6). To induce hypothyroidism, propylthiouracil was added to drinking water at a dosage of 20 mg/kg/day. The test stimulus intensity was calculated, basal recordings were acquired, and LTP was induced by administering 100 Hz high-frequency stimulation (HFS) for 1 second with a 5-minute delay when the rats were aged 60 days. The population spike (PS) amplitude and excitatory postsynaptic potential (EPSP) slope were measured in the granule cell layer of the dentate gyrus. Using reverse transcription polymerase chain reaction, the mRNA levels of neurodegenerative genes were assessed in induced hippocampal tissues after the LTP protocol. The free T4 levels in plasma were measured using a plate reader with the commercial ELISA kit.

Results:  Following HFS, LTP was solely induced in the EPSP slope and PS amplitude in the control group. The impaired LTP response of the hypothyroidism group was accompanied by an increase in Akt1-mRNA expression and a decrease in Gsk3ß expression, whereas the value genes' mRNA expression levels did not difer significantly from those of the control group.

Conclusion:  The hypothyroidism-related LTP impairment could be caused by a reduction in PI3K/AKT signaling. Further investigation of this path is required to elucidate the pathophysiology of impaired synaptic plasticity in hypothyroidism.

甲状腺功能减退大鼠海马体长期电位后神经变性相关基因的表达
研究背景 在我们的研究中,我们考察了甲状腺功能减退大鼠海马中长期电位诱导(LTP)如何影响与神经变性有关的几种蛋白质的mRNA水平,包括Gsk3、Cdk5、Akt1、Mapt、P35(Anxa)、Capn1、Bace1和Psen2: 研究使用了12只雄性Wistar-albino大鼠,将其分为两组:对照组(n=6)和甲减组(n=6)。为了诱导甲减,在饮用水中添加丙基硫氧嘧啶,剂量为 20 毫克/千克/天。计算测试刺激强度,采集基础记录,并在大鼠60天大时给予100赫兹高频刺激(HFS)1秒钟,延迟5分钟,诱导LTP。测量了齿状回颗粒细胞层的群体棘波(PS)振幅和兴奋性突触后电位(EPSP)斜率。通过反转录聚合酶链反应,评估了LTP方案后诱导海马组织中神经退行性基因的mRNA水平。血浆中的游离 T4 含量是通过使用商用酶联免疫吸附试剂盒的平板阅读器测定的: 结果:HFS后,对照组的LTP仅在EPSP斜率和PS振幅上被诱导。甲状腺功能减退症组的LTP反应受损伴随着Akt1-mRNA表达的增加和Gsk3ß表达的减少,而价值基因的mRNA表达水平与对照组没有显著差异: 结论:甲状腺功能减退症相关的LTP损伤可能是由PI3K/AKT信号传导减少引起的。结论:甲减相关的LTP损伤可能是由PI3K/AKT信号的减少引起的,需要对这一途径进行进一步研究,以阐明甲减患者突触可塑性受损的病理生理学。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Eurasian Journal of Medicine
Eurasian Journal of Medicine Medicine-Medicine (all)
CiteScore
1.90
自引率
6.70%
发文量
59
审稿时长
16 weeks
期刊介绍: Eurasian Journal of Medicine (Eurasian J Med) is an international, scientific, open access periodical published by independent, unbiased, and triple-blinded peer-review principles. The journal is the official publication of Atatürk University School of Medicine and published triannually in February, June, and October. The publication language of the journal is English. The aim of the Eurasian Journal of Medicine is to publish original research papers of the highest scientific and clinical value in all medical fields. The Eurasian J Med also includes reviews, editorial short notes and letters to the editor that either as a comment related to recently published articles in our journal or as a case report. The target audience of the journal includes researchers, physicians and healthcare professionals who are interested or working in in all medical disciplines.
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