Institute of Pharmacology, Toxicology, and Pharmacy, Ludwig-Maximilians-University, Koeniginstr. 16, D-80539 Munich, Germany.
Neurosci Lett. 2011 Sep 1;501(3):173-8. doi: 10.1016/j.neulet.2011.07.010. Epub 2011 Jul 20.
Plannexin represents a NCAM-derived peptide mimicking trans-homophilic NCAM interaction, which proved to exert neuroprotective effects in vitro. The effect of plannexin was evaluated in a rat status epilepticus model. As expected, prolonged seizure activity resulted in a pronounced cell loss in hippocampal subregions. The comparison between the vehicle- and plannexin-treated animals with status epilepticus did not reveal neuroprotective effects of plannexin on mature neurons. However, treatment with plannexin partially prevented the reduction in the number of doublecortin-labeled neuronal progenitor cells, which was evident 48h following status epilepticus. In conclusion, the data might give first evidence that plannexin can protect immature neurons in vivo. Future studies are necessary to evaluate whether disease-modifying or preventive effects are observed in models of epileptogenesis.
神经细胞黏附分子衍生肽(Plannexin)模拟了神经细胞黏附分子的同种细胞间相互作用,已被证明具有体外神经保护作用。本研究评估了 Plannexin 在大鼠癫痫持续状态模型中的作用。正如预期的那样,长时间的癫痫发作导致海马亚区明显的细胞丢失。与癫痫持续状态下接受 vehicle 处理的动物相比,接受 Plannexin 处理的动物并未显示出 Plannexin 对成熟神经元的神经保护作用。然而,Plannexin 处理部分预防了癫痫持续状态后 48 小时双皮质素标记的神经祖细胞数量的减少。综上所述,这些数据首次表明 Plannexin 可在体内保护未成熟神经元。未来的研究有必要评估在癫痫发生模型中是否观察到疾病修饰或预防作用。