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Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions
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,...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Pasteur Institute
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075139/ https://www.ncbi.nlm.nih.gov/pubmed/27108691 http://dx.doi.org/10.22045/ibj.2016.03 |
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author | Etemadi, Fatemeh Sayyah, Mohammad Pourbadie, Hamid Gholami Babapour, Vahab |
author_facet | Etemadi, Fatemeh Sayyah, Mohammad Pourbadie, Hamid Gholami Babapour, Vahab |
author_sort | Etemadi, Fatemeh |
collection | PubMed |
description | 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 afterdischarges (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. xx |
format | Online Article Text |
id | pubmed-5075139 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Pasteur Institute |
record_format | MEDLINE/PubMed |
spelling | pubmed-50751392016-11-01 Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions Etemadi, Fatemeh Sayyah, Mohammad Pourbadie, Hamid Gholami Babapour, Vahab Iran Biomed J Full Lenght 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 afterdischarges (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. xx Pasteur Institute 2016-11 /pmc/articles/PMC5075139/ /pubmed/27108691 http://dx.doi.org/10.22045/ibj.2016.03 Text en Copyright: © Iranian Biomedical Journal http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Full Lenght Etemadi, Fatemeh Sayyah, Mohammad Pourbadie, Hamid Gholami Babapour, Vahab Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title_full | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title_fullStr | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title_full_unstemmed | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title_short | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
title_sort | facilitation of hippocampal kindling and exacerbation of kindled seizures by intra-ca1 injection of quinine: a possible role of cx36 gap junctions |
topic | Full Lenght |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075139/ https://www.ncbi.nlm.nih.gov/pubmed/27108691 http://dx.doi.org/10.22045/ibj.2016.03 |
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