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.

中风会导致大脑进入可塑状态。这个可塑性增强的时期导致新轴突的萌芽、新突触的形成和感觉运动功能的重新映射，并与运动恢复相关。这是成人大脑中一个显着的过程，成人大脑通常受到神经元可塑性和连接变化水平的限制。最近的证据表明，这些变化是由学习和记忆基础的分子系统驱动的，例如记忆形成过程中细胞兴奋性的变化。这篇综述研究了中风后的回路变化、记忆形成和大脑修复之间的共同机制、中风恢复背后的神经元兴奋性变化，以及根据这些发现促进动物模型运动恢复的分子和药理学干预措施。根据这些发现，出现了一个理解中风后恢复的框架，其核心是神经元分配到受损回路的概念。中风康复药物的临床试验正在进行中，将这里讨论的概念转化为人类的康复。