Environmental enrichment has been reported to promote functional recovery in an ischemic stroke. However, the underlying mechanism remains unclear. This study aimed to investigate the effect of environmental enrichment treatment on post-ischemic cerebral blood flow and functional hyperemia in the ipsilesional primary somatosensory cortex of rats. With laser speckle imaging, we were able to monitor the resting cerebral blood flow alteration in the middle cerebral artery occlusion model. Both 3- and 28-day post-ischemic infarct volumes were then examined with triphenyltetrazolium chloride and cresyl violet staining, respectively. We found that an exposure to environmental enrichment was associated with higher post-ischemic cerebral blood flow and less brain tissue loss in the ipsilesional primary somatosensory cortex compared with the standard cage environment. Furthermore, environmental enrichment also enhanced the cerebral blood flow response to whisker stimulation in the ipsilesional barrel cortex when measured 28 days after the middle cerebral artery occlusion. Together, the data suggested that an exposure to environmental enrichment promoted the restoration of cerebral blood flow in the ipsilesional cortex and contributed to a better coupling between functional activation and cerebral blood flow change, which might be the possible mechanisms underlying the neuroprotective effects of EE after ischemia.

中文翻译：

---

环境富集增强了同侧躯体感觉皮层的缺血后脑血流量和功能性充血。

据报道，环境丰富可促进缺血性中风的功能恢复。然而，其潜在机制仍不清楚。本研究旨在探讨环境富集治疗对大鼠同侧初级躯体感觉皮层缺血后脑血流量和功能性充血的影响。通过激光散斑成像，我们能够监测大脑中动脉闭塞模型中静息脑血流的变化。然后分别用三苯基四唑氯化物和甲酚紫染色检查缺血后 3 天和 28 天的梗死体积。我们发现，与标准笼子环境相比，暴露于富集环境与较高的缺血后脑血流量和同侧初级躯体感觉皮层中较少的脑组织损失有关。此外，在大脑中动脉闭塞后 28 天测量时，环境富集还增强了大脑血流对同侧桶状皮质中的晶须刺激的反应。总之，这些数据表明，暴露于富集环境促进了同侧皮层脑血流的恢复，并有助于功能激活和脑血流变化之间更好的耦合，这可能是 EE 后神经保护作用的可能机制。缺血。在大脑中动脉闭塞后 28 天测量时，环境富集还增强了大脑血流对同侧桶状皮层中晶须刺激的反应。总之，这些数据表明，暴露于富集环境促进了同侧皮层脑血流的恢复，并有助于功能激活和脑血流变化之间更好的耦合，这可能是 EE 后神经保护作用的可能机制。缺血。在大脑中动脉闭塞 28 天后测量时，环境富集还增强了大脑血流对同侧桶状皮层中晶须刺激的反应。总之，这些数据表明，暴露于富集环境促进了同侧皮层脑血流的恢复，并有助于功能激活和脑血流变化之间更好的耦合，这可能是 EE 后神经保护作用的可能机制。缺血。