ArticleIranian biomedical journal2016
Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions.
Article in Iranian biomedical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Hippocampal Expression of Connexin36 and Connexin43 during Epileptogenesis in Pilocarpine Model of Epilepsy.Iranian biomedical journal · 2017Article
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundGABAergic 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.
methodsQuinine, 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.
resultsQuinine 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 afterdischarges (AD) were also significantly increased. Quinine 0.1 mM augmented the rate of kindling and the growth of secondary AD.
conclusionCx36 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.
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