ABSTRACT
Background: Gap junctions [GJs] provide direct intercellular communications that are formed by hexameric protein subunits, called connexin [Cx]. The role of Cxs in epileptogenesis has not received sufficient attention. Hippocampus with critical function in epileptogenesis has a wide network of GJs. We examined the protein expression levels of hippocampal Cx36 [the prominent Cx present between GABAergic interneurons] and Cx43 [the main Cx expressed by astrocytes] during epileptogenesis in the pilocarpine model of epilepsy
Methods: Male Wistar rats received scopolamine [1 mg/kg, s.c.]. Pilocarpine [380 mg/kg, i.p.] was administered 30 min thereafter to induce status epilepticus [SE]. SE was stopped 2 h later by diazepam [10 mg/kg, i.p.]. Cx36 and Cx43 protein expression was assessed by Western blot analysis in the hippocampus of SE-experienced rats, after injection of diazepam [F0 subgroup], after acquisition of focal seizures [F3 subgroup], and after development of generalized seizures [F5 subgroup]. The control subgroups, C0, C3, and C5, were aged-matched rats, which received saline [1 ml/kg, i.p.] instead of pilocarpine. Injection of scopolamine and diazepam, and dissection of hippocampi were carried out at the same time interval as the test subgroups
Results: SE emerged in 67.1% of pilocarpine-treated animals. Focal and generalized seizures developed 3.8 +/- 0.4 and 7.0 +/- 0.5 days after SE, respectively. Cx36 protein abundance was not significantly different between test and control groups in the three time points. However, Cx43 protein level showed 40% increase in F3 subgroup [P<0.05 compared to C3, P<0.01 compared to F0 and F5]
Conclusion: Hippocampal Cx43 is overexpressed in pilocarpine model of epileptogenesis after acquisition of focal seizures