Blocking of rat hippocampal Cx36 by quinine accelerates kindling epileptogenesis

Authors

  • Jafar Kazemi Ghanbarabadi Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran; Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran
  • Mohammad Sayyah Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran

Keywords:

Cx36, CA1, amygdala kindling, quinine

Abstract

There are abundant studies indicating that blocking gap junctions (GJs) containing connexin 36 (Cx36) inhibit seizures. However, recent evidences demonstrate proconvulsant effect of such intervention. Electrical coupling between GABAergic interneurons in CA1 region of hippocampus is mediated through Cx36 GJs. We investigated effect of quinine, a specific blocker of Cx36, on the seizure severity and epileptogenesis in amygala kindling model of epilepsy in rats. Quinine (1, 50, 100, 500 and 2000 µM/rat) was injected directly into the CA1 and kindled seizure parameters including behavioral seizure stage, duration of evoked afterdischarges, and duration of generalized seizures behavior were recorded 10 min afterward. Moreover, quinine (1, 30, and 100 µM/rat) was injected intra CA1 once daily during kindling development. At the doses used, quinine had no significant effect on amygdala-kindled seizures. However, quinine 100 µM significantly accelerated kindling rate. Blockade of Cx36 GJs coupling and consequent disruption of inhibitory transmission in GABAergic interneurons in CA1 area seems to be responsible for the antiepileptogenic effect of quinine.

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Published

2013-03-14

How to Cite

Ghanbarabadi, J. K., & Sayyah, M. (2013). Blocking of rat hippocampal Cx36 by quinine accelerates kindling epileptogenesis. EXCLI Journal, 12, 251–259. Retrieved from https://www.excli.de/index.php/excli/article/view/1146

Issue

Vol. 12 (2013)

Section

Original articles

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