Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA.
Nat Rev Neurosci. 2021 Jan;22(1):38-53. doi: 10.1038/s41583-020-00396-7. Epub 2020 Nov 12.
Stroke induces a plastic state in the brain. This period of enhanced plasticity leads to the sprouting of new axons, the formation of new synapses and the remapping of sensory-motor functions, and is associated with motor recovery. This is a remarkable process in the adult brain, which is normally constrained in its levels of neuronal plasticity and connectional change. Recent evidence indicates that these changes are driven by molecular systems that underlie learning and memory, such as changes in cellular excitability during memory formation. This Review examines circuit changes after stroke, the shared mechanisms between memory formation and brain repair, the changes in neuronal excitability that underlie stroke recovery, and the molecular and pharmacological interventions that follow from these findings to promote motor recovery in animal models. From these findings, a framework emerges for understanding recovery after stroke, central to which is the concept of neuronal allocation to damaged circuits. The translation of the concepts discussed here to recovery in humans is underway in clinical trials for stroke recovery drugs.
中风会使大脑进入一种可塑状态。这段增强的可塑性期会导致新轴突的生长、新突触的形成和感觉运动功能的重新映射，与运动功能的恢复有关。这是成年人大脑中一个显著的过程，在正常情况下，神经元的可塑性和连接变化受到限制。最近的证据表明，这些变化是由学习和记忆的分子系统驱动的，例如在记忆形成过程中细胞兴奋性的变化。这篇综述探讨了中风后的回路变化、记忆形成和大脑修复之间的共享机制、中风恢复所依赖的神经元兴奋性变化，以及从这些发现中得出的分子和药理学干预措施，以促进动物模型中的运动功能恢复。从这些发现中，出现了一个理解中风后恢复的框架，其中的核心概念是神经元对受损回路的分配。这里讨论的概念在中风恢复药物的临床试验中正在向人类的恢复转化。
