PDF(Pubmed)
Abstract：
Ischemic stroke can cause depolarized brain waves, termed peri-infarct depolarization (PID). Here, we evaluated whether topiramate, a neuroprotective drug used to treat epilepsy and alleviate migraine, has the potential to reduce PID. We employed a rat model of photothrombotic ischemia that can reliably and reproducibly induce PID and developed a combined electrocorticography-laser speckle contrast imaging (ECoG-LSCI) platform to monitor neuronal activity and cerebral blood flow (CBF) simultaneously. Topiramate administration after photothrombotic ischemia did not rescue CBF but significantly restored somatosensory evoked potentials in the forelimb area of the primary somatosensory cortex. Moreover, infarct volume was investigated by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and neuronal survival was evaluated by Nissl staining. Mechanistically, the levels of inflammatory markers, such as ED1 (CD68), Iba-1, and GFAP, decreased significantly after topiramate administration, as did BDNF expression, while the expression of NeuN and Bcl-2/Bax increased, which is indicative of reduced inflammation and improved neuroprotection.
摘要：
缺血性中风会导致脑电波去极化,称为梗死周围去极化（PID）。这里,我们评估了托吡酯,一种用于治疗癫痫和缓解偏头痛的神经保护药物，有可能降低PID。我们采用了一种可以可靠且可重复地诱导PID的光血栓性缺血大鼠模型，并开发了一种联合的脑电图-激光散斑对比成像（ECoG-LSCI）平台，以同时监测神经元活动和脑血流量（CBF）。光血栓性缺血后施用托吡酯不能挽救CBF，但显着恢复了原发性体感皮层前肢区域的体感诱发电位。此外，通过氯化2,3,5-三苯基四唑（TTC）染色研究梗死体积，通过Nissl染色评估神经元存活。机械上,炎症标志物的水平，如ED1(CD68)，Iba-1和GFAP，服用托吡酯后显著下降，BDNF表达也是如此，而NeuN和Bcl-2/Bax的表达增加,这表明炎症减少和神经保护改善。
