Department of Animal Biology, School of Biology, University College of Science, Tehran University, Tehran, Iran.
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Apr 16;34(3):510-5. doi: 10.1016/j.pnpbp.2010.02.006. Epub 2010 Feb 12.
Identification of key molecular changes occurring during epileptogenesis provides better understanding of epilepsy and helps to develop strategies to modify those changes and thus, block the epileptogenic process. Gap junctional communication is thought to be involved in epileptogenesis. This communication can be affected by changes in expression of gap junctional protein subunits called connexins (Cxs). One of the main brain regions involved in epileptogenesis is the hippocampus in which there is a network of gap junctional communication between different cell types.
Cx36 and Cx43 expressions at both mRNA and protein level were measured in rat hippocampus during epileptogenesis in the kindling model of epilepsy.
Cx36 expression at both mRNA and protein level was upregulated during acquisition of focal seizures but returned to basal level after acquisition of secondarily-generalized seizures. No change in Cx43 gene and protein expression was found during kindling epileptogenesis.
These results further point out the significance of Cx36 as a target to modify epileptogenic process and to develop antiepileptogenic treatments.
识别癫痫发生过程中发生的关键分子变化，更好地了解癫痫，并有助于制定策略来改变这些变化，从而阻断致痫过程。缝隙连接通讯被认为与癫痫发生有关。这种通讯可以通过连接蛋白（Cxs）亚基表达的变化来影响。在癫痫发生中涉及的主要脑区之一是海马体，其中不同细胞类型之间存在缝隙连接通讯网络。
在癫痫点燃模型中，测量大鼠海马体在癫痫发生过程中 Cx36 和 Cx43 在 mRNA 和蛋白水平的表达。
在获得局灶性发作期间，Cx36 在 mRNA 和蛋白水平的表达均上调，但在获得继发性全身性发作后恢复到基础水平。在点燃癫痫发生过程中未发现 Cx43 基因和蛋白表达的变化。
这些结果进一步指出 Cx36 作为改变致痫过程和开发抗癫痫治疗的靶点的重要性。
