Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy

作     者：Bijan Akbarpour Mohammad Sayyah Vahab Babapour Reza Mahdian Siamak Beheshti Ahmad Reza Kamyab 

作者机构：Departments of Physiology and PharmacologyPasteur Institute of Iran.Tehran 131694-3551Islamic Republic of Iran Department of PhysiologyFaculty of Veterinary MedicineIslamic Azad UniversityScience and Research BranchTehran 14778-93855Islamic Republic of Iran Departments of Physiology and PharmacologyPasteur Institute of IranTehran 131694-3551Islamic Republic of Iran Department of PhysiologyFaculty of Veterinary MedicineTehran UniversityTehran 141996-31111Islamic-Republic of Iran Department of Molecular MedicineBiotechnology Research CenterPasteur Institute of Iran Department of Biology Faculty of ScienceUniversity of IsfahanIsfahan 81746-73441Islamic Republic of Iran 

出 版 物：《Neuroscience Bulletin》 (神经科学通报（英文版）)

年 卷 期：2012年第28卷第6期

页      面：729-736页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

主　　题：connexin 30 connexin 32 hippocampus kindling 

摘      要：Objective Understanding the molecular and cellular mechanisms underlying epileptogenesis yields new in- sights into potential therapies that may ultimately prevent epilepsy. Gap junctions （GJs） create direct intercellular conduits between adjacent cells and are formed by hexameric protein subunits called connexins （Cxs）. Changes in the expression of Cxs affect GJ communication and thereby could modulate the dissemination of electrical discharges. The hippocampus is one of the main regions involved in epileptogenesis and has a wide network of GJs between different cell types where Cx30 is expressed in astrocytes and Cx32 exists in neurons and oligodendrocytes. In the present study, we evaluated the changes of Cx30 and Cx32 expression in rat hippocampus during kindling epileptogenesis. Methods Rats were stereotaxically implanted with stimulating and recording electrodes in the basolateral amygdala, which was electrically stimulated once daily at afterdischarge threshold. Expression of Cx30 and Cx32, at both the mRNA and protein levels, was measured in the hippocampus at the beginning, in the middle （after acquisition of focal seizures）, and at the end （after establishment of generalized seizures） of the kindling process, by real-time PCR and Western blot. Results Cx30 mRNA expression was upregulated at the beginning of kindling and after acquisition of focal seizures. Then it was downregulated when the animals acquired generalized seizures. Overexpression of Cx30 mRNA at the start of kindling was consistent with the respective initial protein increase. Thereafter, no change was found in protein abundance during kindling. Regarding Cx32, mRNA expression decreased after acquisition of generalized seizures and no other significant change was detected in mRNA and protein abundance during kindling. Conclusion We speculate that Cx32 GJ communication in the hip- pocampus does not contribute to kindling epileptogenesis. The Cx30 astrocytic network localized to perivascular regions in the hippocampus is, however, overexpressed at the initiation of kindling to clear excitotoxic molecules from the milieu.