甲状腺功能障碍症诱导的神经退行相关基因表达的升高调节在转塑性诱导的海马体中
Ercan Babur1, Melek Altunkaya2, Esra Tufan3
1Department of Physiology, Erciyes University Faculty of Medicine, Kayseri, Turkey, ercanbabur@erciyes.edu.tr.
Neuroendocrinology
|January 3, 2024
概括
鼠类甲状腺功能障碍改变了与神经退行相关的基因表达,尽管甲型可塑性反应仍然与正常水平相似. 这表明甲状腺激素过量与神经退行性疾病风险增加之间存在潜在联系.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 甲状腺激素调节基因转录,对生理功能至关重要.
- 神经元可塑性涉及蛋白质合成和基因表达,以应对外部刺激.
- 甲状腺功能障碍对转移性长期强化 (LTP) 和基因表达的影响仍然未被探索.
研究的目的:
- 为了研究甲基可塑性和基因表达变化在海马的甲状腺功能过高的小鼠模型.
- 为了确定甲状腺功能障碍是否影响长期潜能 (LTP) 和相关基因表达.
主要方法:
- 在Wistar雄性大鼠中使用l-甲状腺素诱导甲状腺功能过高.
- 使用低频刺激 (LFS),然后使用高频刺激 (HFS) 评估了转塑性.
- 测量了电生理反应 (EPSP斜率,PS振幅) 和与神经退行相关基因的mRNA水平.
主要成果:
- 甲状腺功能过高的小鼠表现出与甲状腺功能良好的小鼠相似的转移性LTP反应.
- 尽管有电生理学上的相似之处,但甲状腺功能高的小鼠显示了Akt1,Bace1,Cdk5和p35.5的mRNA表达增加.
- 在甲状腺功能高大鼠中观察到Gsk-3βmRNA表达的减少.
结论:
- 过多的甲状腺激素可能涉及维持突触功效的机制,同时升调神经退行相关基因表达.
- 这些发现突出了甲状腺功能障碍和神经退行性疾病风险增加之间的潜在关联.
- 需要进一步的研究来探索这种联系.
更多相关视频
09:46Analysis of Gene Expression Changes in the Rat Hippocampus After Deep Brain Stimulation of the Anterior Thalamic Nucleus
Published on: March 8, 2015
11.0K
07:43Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
Published on: May 12, 2015
11.3K
相关概念视频
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...