Data from: Protein synthesis inhibition in the peri-infarct cortex slows motor recovery in rats

Neuroplasticity and reorganization of brain motor networks are thought to enable recovery of motor function after ischemic stroke. Especially in the cortex surrounding the ischemic scar (i.e., peri-infarct cortex), evidence for lasting reorganization has been found at the level of neurons and networks. This reorganization depends on expression of specific genes and subsequent protein synthesis. To test the functional relevance of the peri-infarct cortex for recovery we assessed the effect of protein synthesis inhibition within this region after experimental stroke. Long-Evans rats were trained to perform a skilled-reaching task (SRT) until they reached plateau performance. A photothrombotic stroke was induced in the forelimb representation of the primary motor cortex (M1) contralateral to the trained paw. The SRT was re-trained after stroke while the protein synthesis inhibitor anisomycin (ANI) or saline were injected into the peri-infarct cortex through implanted cannulas. ANI injections reduced protein synthesis within the peri-infarct cortex by 69% and significantly impaired recovery of reaching performance through re-training. Improvement of motor performance within a single training session remained intact, while improvement between training sessions was impaired. ANI injections did not affect infarct size. Thus, protein synthesis inhibition within the peri-infarct cortex impairs recovery of motor deficits after ischemic stroke by interfering with consolidation of motor memory between training sessions but not short-term improvements within one session.

大脑运动网络的神经可塑性与重塑被认为可介导缺血性脑卒中（ischemic stroke）后运动功能的恢复。尤其在缺血瘢痕周边的皮层（即梗死周围皮层（peri-infarct cortex）），已有研究在神经元及神经网络层面证实了持久性重塑的存在。此类重塑依赖于特定基因的表达与后续蛋白质合成过程。为验证梗死周围皮层对运动功能恢复的功能性价值，本研究在实验性脑卒中模型中，检测了该区域内蛋白质合成抑制对恢复进程的影响。
将Long-Evans大鼠训练至熟练抓取任务（skilled-reaching task, SRT）的性能达到平台期后，在其训练用后肢对侧的初级运动皮层（primary motor cortex, M1）前肢代表区诱导光血栓性脑卒中。脑卒中后，大鼠接受SRT再训练，同时通过植入的套管向梗死周围皮层内注射蛋白质合成抑制剂茴香霉素（anisomycin, ANI）或生理盐水。
注射ANI可使梗死周围皮层内的蛋白质合成水平降低69%，并显著损害了再训练过程中抓取能力的恢复。单一场次训练周期内的运动性能改善得以保留，但跨训练周期的性能提升则受到抑制。ANI注射并未对梗死体积产生影响。
综上，梗死周围皮层内的蛋白质合成抑制会通过干扰训练周期间的运动记忆巩固过程，而非单一场训练内的短期性能提升，损害缺血性脑卒中后运动功能缺损的恢复。