Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Germany.
Brain Res. 2012 Oct 15;1479:80-5. doi: 10.1016/j.brainres.2012.08.046. Epub 2012 Aug 31.
Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs. In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined. Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia. These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.
皮质扩散性抑制（CSD）可促进脑缺血后神经元损伤的进展。然而，缺血后 CSD 事件传播的机制仍不清楚。在这项研究中，我们描述了主要神经元缝隙连接蛋白连接蛋白 36（Cx36）在产生缺血后 CSD 中的作用。在 Cx36 缺陷小鼠和对照小鼠中，我们阻断了大脑中动脉的远端。为了检测 CSD 事件，我们记录了直流和激光多普勒流量。此外，还确定了运动功能和梗死面积。Cx36 缺陷小鼠的 CSD 事件明显少于野生型对照小鼠。此外，Cx36 缺失具有神经保护作用，可导致缺血后功能结局更好，梗死面积减小。这些结果表明，Cx36 在缺血后可能具有有害作用，可能通过促进 CSD 而发挥作用。
