Department of Psychology, University of Otago, PO Box 56, Dunedin, 9054, New Zealand.
Department of Anatomy, Brain Health Research Centre and Brain Research New Zealand, University of Otago, PO Box 56, Dunedin, 9054, New Zealand.
Neuromolecular Med. 2019 Dec;21(4):401-413. doi: 10.1007/s12017-019-08557-3. Epub 2019 Jul 16.
Frontal infarcts can produce cognitive impairments that affect an individual's ability to function in everyday life. However, the precise types of deficits, and their underlying mechanisms, are not well-understood. Here we used a prefrontal photothrombotic stroke model in C57BL/6J mice to characterise specific cognitive changes that occur in the 6 weeks post-stroke. Behavioural experiments were paired with in vivo electrophysiology to assess whether changes in oscillatory communication between the prefrontal cortex (PFC) and the hippocampus (HPC) mirrored any observed behavioural changes. We found that mice in the stroke group exhibited a delayed onset impairment in tasks of spatial working memory (object location recognition and Y-maze) and that this correlated with reduced PFC-HPC theta band coherence (5-12 Hz) during the task. In the open field, mice in the stroke group exhibited hyperactivity as compared to controls, and stroke animals also exhibited significantly higher beta band activity (13-30 Hz) in the PFC and the HPC. Taken together our results suggest that infarcts in the PFC result in PFC-HPC oscillatory communication changes in the theta and beta bands, correlating with altered performance in spatial memory and open field tasks respectively. Of particular interest, early open field changes in PFC beta band power post-stroke correlated to later-stage spatial memory impairments, highlighting this as a potential biomarker for detecting when spatial memory impairments are likely to occur.
额叶梗死可导致认知障碍，影响个体日常生活的功能。然而，确切的缺陷类型及其潜在机制尚不清楚。在这里，我们使用 C57BL/6J 小鼠的前额叶光血栓形成中风模型来描述中风后 6 周内发生的特定认知变化。行为实验与体内电生理学相结合，以评估前额叶皮层 (PFC) 和海马体 (HPC) 之间的振荡通讯变化是否反映了任何观察到的行为变化。我们发现，中风组的小鼠在空间工作记忆任务（物体位置识别和 Y 迷宫）中表现出延迟发作的损伤，并且这与任务期间 PFC-HPC theta 波段相干性（5-12 Hz）降低相关。在开阔场中，与对照组相比，中风组的小鼠表现出过度活跃，并且中风动物在 PFC 和 HPC 中也表现出显著更高的 beta 波段活动（13-30 Hz）。总的来说，我们的结果表明，PFC 中的梗死导致 PFC-HPC 中的 theta 和 beta 波段的振荡通讯变化，分别与空间记忆任务和开阔场任务的表现改变相关。特别有趣的是，中风后 PFC 中 beta 波段功率的早期开阔场变化与后期空间记忆损伤相关，这突出了这一点作为检测空间记忆损伤何时可能发生的潜在生物标志物。
