Division of Medical Sciences, University of Victoria, Victoria, BC, Canada.
Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, Italy.
Adv Neurobiol. 2024;37:221-242. doi: 10.1007/978-3-031-55529-9_13.
Neural plasticity can be defined as the ability of neural circuits to be shaped by external and internal factors. It provides the brain with a capacity for functional and morphological remodelling, with many lines of evidence indicating that these changes are vital for learning and memory formation. The basis of this brain plasticity resides in activity- and experience-driven modifications of synaptic strength, including synaptic formation, elimination or weakening, as well as of modulation of neuronal population, which drive the structural reorganization of neural networks. Recent evidence indicates that brain-resident glial cells actively participate in these processes, suggesting that mechanisms underlying plasticity in the brain are multifaceted. Establishing the 'tripartite' synapse, the role of astrocytes in modulating synaptic transmission in response to neuronal activity was recognized first. Further redefinition of the synapse as 'quad-partite' followed to acknowledge the contribution of microglia which were revealed to affect numerous brain functions via dynamic interactions with synapses, acting as 'synaptic sensors' that respond to neuronal activity and neurotransmitter release, as well as crosstalk with astrocytes. Early studies identified microglial ability to dynamically survey their local brain environment and established their integral role in the active interfacing of environmental stimuli (both internal and external), with brain plasticity and remodelling. Following the introduction to neurogenesis, this chapter details the role that microglia play in regulating neurogenesis in adulthood, specifically as it relates to learning and memory, as well as factors involved in modulation of microglia. Further, a microglial perspective is introduced for the context of environmental enrichment impact on neurogenesis, learning and memory across states of stress, ageing, disease and injury.
神经可塑性可以被定义为神经回路被外部和内部因素塑造的能力。它为大脑提供了功能和形态重塑的能力，有许多证据表明这些变化对于学习和记忆的形成至关重要。这种大脑可塑性的基础在于突触强度的活动和经验驱动的改变，包括突触的形成、消除或减弱，以及神经元群体的调节，这些改变驱动了神经网络的结构重组。最近的证据表明，脑内胶质细胞积极参与这些过程，这表明大脑可塑性的机制是多方面的。首先认识到星形胶质细胞在调节突触传递以响应神经元活动中的作用，确立了“三分叉”突触。随后，对突触进行了重新定义，将其称为“四分叉”，以承认小胶质细胞的作用，小胶质细胞通过与突触的动态相互作用，影响着许多大脑功能，作为“突触传感器”，可以响应神经元活动和神经递质释放，并与星形胶质细胞进行交流。早期研究发现小胶质细胞能够动态地监测其局部脑环境，并确立了它们在环境刺激（内部和外部）与大脑可塑性和重塑的积极接口中的不可或缺的作用。在介绍神经发生之后，这一章详细介绍了小胶质细胞在调节成年期神经发生中的作用，特别是与学习和记忆有关的作用，以及调节小胶质细胞的相关因素。此外，还引入了一个从小胶质细胞的角度来看待环境富集对神经发生、学习和记忆的影响，以及在应激、衰老、疾病和损伤状态下的影响。
