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在多发性硬化症的动物模型中,海马神经元的结构可塑性的变化

Poornima D E Weerasinghe-Mudiyanselage¹, Sohi Kang^1,2, Joong-Sun Kim¹

¹Department of Veterinary Anatomy and Animal Behavior, College of Veterinary Medicine and BK21 FOUR Program, Chonnam National University, Gwangju 61186, Republic of Korea.

Zoological research

|March 14, 2024

概括

实验性自身免疫脑膜炎 (EAE),多发性硬化症的一个模型,损害了海马体的结构性可塑性和功能. 在EAE中的神经炎症会改变树突复杂性和脊柱密度,影响大脑功能.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

结构性可塑性对于神经元功能和大脑多样性至关重要.
实验性自身免疫脑膜炎 (EAE) 模型多发性硬化症 (MS) 病理和症状.
突触可塑性变化与EAE病变发生有关.

研究的目的:

在早期和慢性阶段研究EAE小鼠的行为变化和海马结构可塑性.
探索神经炎症诱导的可塑性变化背后的分子机制.

主要方法:

在EAE小鼠中进行行为测试 (开放场地测试).
在海马子区域 (CA1,CA3,DG) 的树突复杂性和脊柱密度的分析.
测量细胞因子和质标记物mRNA水平,以及ARC表达.
在实验室中对暴露于益炎性细胞因子的原发性海马神经元进行研究.

主要成果:

在早期和慢性阶段,EAE小鼠表现出海马体依赖的行为缺陷.
在慢性阶段,海马体亚区域的树突复杂性减少,在早期阶段的CA1.
在早期阶段,多个海马子子区域的状脊柱密度下降,在慢性阶段的DG.
预炎性细胞因子和质标记物增加,而慢性EAE中ARC表达减少.
在体外细胞因子暴露减少了树突复杂性,ARC表达和ERK酸化.

结论:

在EAE中,自身免疫神经炎症会改变海马体的结构性可塑性.
ERK-ARC路径可能会调解这些可塑性变化.
海马结构变化与EAE的功能缺陷有关.

关键词:

活动调节的细胞骨相关蛋白质.类似焦虑的行为.实验性的自身免疫性脑膜炎.河马的功能障碍河马的功能障碍神经炎症是一种神经炎症.

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Neuroplasticity

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.