Section of Neurology, Department of Medicine and Surgery, Università degli Studi di Perugia, Perugia, Italy.
Università Telematica San Raffaele, Rome, Italy.
Front Immunol. 2021 Apr 19;12:644294. doi: 10.3389/fimmu.2021.644294. eCollection 2021.
The basal ganglia network is represented by an interconnected group of subcortical nuclei traditionally thought to play a crucial role in motor learning and movement execution. During the last decades, knowledge about basal ganglia physiology significantly evolved and this network is now considered as a key regulator of important cognitive and emotional processes. Accordingly, the disruption of basal ganglia network dynamics represents a crucial pathogenic factor in many neurological and psychiatric disorders. The striatum is the input station of the circuit. Thanks to the synaptic properties of striatal medium spiny neurons (MSNs) and their ability to express synaptic plasticity, the striatum exerts a fundamental integrative and filtering role in the basal ganglia network, influencing the functional output of the whole circuit. Although it is currently established that the immune system is able to regulate neuronal transmission and plasticity in specific cortical areas, the role played by immune molecules and immune/glial cells in the modulation of intra-striatal connections and basal ganglia activity still needs to be clarified. In this manuscript, we review the available evidence of immune-based regulation of synaptic activity in the striatum, also discussing how an abnormal immune activation in this region could be involved in the pathogenesis of inflammatory and degenerative central nervous system (CNS) diseases.
基底神经节网络由一组相互连接的皮层下核团组成，传统上认为这些核团在运动学习和运动执行中起着至关重要的作用。在过去的几十年中，人们对基底神经节生理学的认识有了显著的发展，现在认为该网络是重要认知和情绪过程的关键调节者。因此，基底神经节网络动力学的破坏是许多神经和精神疾病的关键致病因素。纹状体是该回路的输入站。由于纹状体中间神经元（MSNs）的突触特性及其表达突触可塑性的能力，纹状体在基底神经节网络中发挥着基本的整合和过滤作用，影响整个回路的功能输出。尽管目前已经确定免疫系统能够调节特定皮层区域的神经元传递和可塑性，但免疫分子和免疫/神经胶质细胞在调节纹状体内连接和基底神经节活动中的作用仍有待阐明。在本文中，我们回顾了关于免疫调节纹状体内突触活动的现有证据，还讨论了该区域异常免疫激活如何参与炎症和退行性中枢神经系统（CNS）疾病的发病机制。
