ABSTRACT
Background: GABAergic interneurons in the hippocampal CA1 area are mutually communicated by gap junctions [GJs] composed of connexin36 [Cx36]. We examined the role of Cx36 in CA1 in manifestation of kindled seizures and hippocampal kindling in rats
Methods: Quinine, as the specific blocker of Cx36, was injected into CA1, and kindled seizures severity was examined 10 min afterward. Moreover, quinine was injected into CA1 once daily, and the rate of CA1 kindling was recorded
Results: Quinine 0.5 and 1 mM caused 2- and 3.5-fold increase in the duration of total seizure behavior and generalized the seizures. Primary and secondary after discharges [AD] were also significantly increased. Quinine 0.1 mM augmented the rate of kindling and the growth of secondary AD
Conclusion: Cx36 GJs in CA1 are the main components of hippocampal inhibitory circuit. Any interruption in this path by pathologic or physical damages can trigger hippocampal hyperexcitability and facilitate epileptogenesis