Role of gap junction in pentylenetetrazol-induced epilepsy in rats

AIM: To study the role of gap junction(GJ) in the pathogenesis of epilepsy. METHODS: The expression of connexin(Cx) 32 and Cx43 was evaluated in penlylenetetrazol(PTZ)-induced epilepsy rats at different time points with immunohistochemistry and real-time RT-PCR. The uncoupler of gap junction,carbenoxolone (CBX), and anti-epilepsy drug,carbamazepine (CBZ), were introduced to investigate the role of gap junction in epilepsy. RESULTS: The expression of Cx32 in the cortex and hippocampus of rats increased 2 h after PTZ administration, and was more obvious 8 h later, so was the expression of Cx43. CBX not only notably inhibited the expression of Cx32 and Cx43, but also suppressed the seizures. CBZ had no obvious effect on Cx32/43 expression. Real-time RT-PCR examination showed that the level of Cx32 mRNA went up rapidly 2 h after seizures, and began to decrease 10 h later. The level of Cx43 mRNA in PTZ group was higher than that in control group from 2 h to 5 h. CBX inhibited both the seizures and the increase in the mRNA expression of Cx32/43, while CBZ only suppressed the seizures and did not affect the expression of Cx32/43. CONCLUSION: GJ between neurons is reinforced after epileptic activities and takes part in the pathophysiological mechanism of synchronization and epilepsy. CBZ has no effect on the expression of Cx32 and Cx43, indicating that the anti-epileptic mechanism of CBZ is independent of GJ.