Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, 79104 Freiburg, Germany.
Center Brain Links Brain Tools, University of Freiburg, 79110 Freiburg, Germany.
Biomolecules. 2021 Feb 26;11(3):359. doi: 10.3390/biom11030359.
Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood-brain interface, i.e., the blood-brain barrier, in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes plasticity and modulates vascular function, we argue that clinically employed non-invasive brain stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and modulating inflammation-induced alterations in synaptic plasticity.
中枢神经系统炎症可由内源性和外源性刺激引发，如局部或全身感染、创伤和中风等。除了神经退行性变和细胞死亡外，生理脑功能的改变通常与神经炎症有关。大量实验证据表明，炎症细胞因子会影响神经元表达可塑性的能力。已经证实，与炎症相关的突触可塑性改变有助于神经精神症状的发展。然而，用于恢复突触可塑性炎症缺陷的诊断方法和干预策略非常有限。在这里，我们回顾了关于炎症相关突触可塑性改变的最新发现，以及血脑界面（即血脑屏障）在调节突触可塑性方面的潜在作用。基于最近的研究结果表明，大脑刺激可以促进可塑性并调节血管功能，我们认为临床上使用的非侵入性大脑刺激技术，如经颅磁刺激，可以用于监测和调节炎症引起的突触可塑性改变。
