Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions
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. Quinine, as the specific blocker of Cx36, was injected into CA...
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| Veröffentlicht in: | Iranian biomedical journal 2016-11, Vol.20 (5), p.266-272 |
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| creator | Etemadi, Fatemeh Sayyah, Mohammad Gholami Pourbadie, Hamid Babapour, Vahab |
| description | 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.
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.
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.
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. |
| doi_str_mv | 10.22045/ibj.2016.03 |
| format | Article |
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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.
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.
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.</description><identifier>ISSN: 1028-852X</identifier><identifier>EISSN: 2008-823X</identifier><identifier>DOI: 10.22045/ibj.2016.03</identifier><identifier>PMID: 27108691</identifier><language>eng</language><publisher>Iran: Pasteur Institute of Iran</publisher><subject>Animals ; Connexins - metabolism ; Epilepsy ; Full Lenght ; Gap Junction delta-2 Protein ; Gap Junctions - drug effects ; Gap Junctions - metabolism ; Hippocampus - drug effects ; Hippocampus - physiopathology ; Histology ; Kindling, Neurologic - drug effects ; Male ; Quinine - pharmacology ; Rats ; Rats, Wistar ; Rodents ; Seizures - physiopathology ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology</subject><ispartof>Iranian biomedical journal, 2016-11, Vol.20 (5), p.266-272</ispartof><rights>Copyright Pasteur Institute of Iran Nov 2016</rights><rights>Copyright: © Iranian Biomedical Journal 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075139/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075139/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27108691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Etemadi, Fatemeh</creatorcontrib><creatorcontrib>Sayyah, Mohammad</creatorcontrib><creatorcontrib>Gholami Pourbadie, Hamid</creatorcontrib><creatorcontrib>Babapour, Vahab</creatorcontrib><title>Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions</title><title>Iranian biomedical journal</title><addtitle>Iran Biomed J</addtitle><description>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.
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.
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.
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.</description><subject>Animals</subject><subject>Connexins - metabolism</subject><subject>Epilepsy</subject><subject>Full Lenght</subject><subject>Gap Junction delta-2 Protein</subject><subject>Gap Junctions - drug effects</subject><subject>Gap Junctions - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiopathology</subject><subject>Histology</subject><subject>Kindling, Neurologic - drug effects</subject><subject>Male</subject><subject>Quinine - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Seizures - physiopathology</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><issn>1028-852X</issn><issn>2008-823X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkUtv1DAUhS0EokPLjjWyxIZNhms7frFAGo36pBLlJXUXOclN8Shjp3GCWn4Gvxi3tBWwYnN9pPPdoyNfQl4wWHIOpXzj682SA1NLEI_IggOYwnBx_pgsGPCsJT_fIc9S2gAIybR-Sna4ZmCUZQvy88A1vveTm3wMNHb0yA9DbNx2cD1970Pb-3BBXWjp_pVrcKwfwFsTW_oZ_Y95xETra3ocptEV6xXLaoPNPfpx9sEHfEtX9Cym5Ose6aeYR_bWV0LRQzfQkzncLqQ98qRzfcLnd-8u-Xqw_2V9VJx-ODxer06LgZd8Ksq6tNyVHWOl7iS2pWCiRANZdg1oYBpKVSspEa2D2lhrW9eKTlgDyIUUu-Td79xhrrfYNnhTvq-G0W_deF1F56u_neC_VRfxeyVBSyZsDnh9FzDGyxnTVG19arDvXcA4p4qZTBrFrPoPlDNteb5KRl_9g27iPIb8E5kSyippNGTq5Z_lH1rfX1b8AhHKpQc</recordid><startdate>201611</startdate><enddate>201611</enddate><creator>Etemadi, Fatemeh</creator><creator>Sayyah, Mohammad</creator><creator>Gholami Pourbadie, Hamid</creator><creator>Babapour, Vahab</creator><general>Pasteur Institute of Iran</general><general>Pasteur Institute</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QO</scope><scope>7T5</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201611</creationdate><title>Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions</title><author>Etemadi, Fatemeh ; Sayyah, Mohammad ; Gholami Pourbadie, Hamid ; Babapour, Vahab</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p242t-4b492a4f1147f5ed43134e805edfc07017046b655ee9a0b8999dad3f3980e2353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Connexins - metabolism</topic><topic>Epilepsy</topic><topic>Full Lenght</topic><topic>Gap Junction delta-2 Protein</topic><topic>Gap Junctions - drug effects</topic><topic>Gap Junctions - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiopathology</topic><topic>Histology</topic><topic>Kindling, Neurologic - drug effects</topic><topic>Male</topic><topic>Quinine - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Seizures - physiopathology</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Etemadi, Fatemeh</creatorcontrib><creatorcontrib>Sayyah, Mohammad</creatorcontrib><creatorcontrib>Gholami Pourbadie, Hamid</creatorcontrib><creatorcontrib>Babapour, Vahab</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Iranian biomedical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Etemadi, Fatemeh</au><au>Sayyah, Mohammad</au><au>Gholami Pourbadie, Hamid</au><au>Babapour, Vahab</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions</atitle><jtitle>Iranian biomedical journal</jtitle><addtitle>Iran Biomed J</addtitle><date>2016-11</date><risdate>2016</risdate><volume>20</volume><issue>5</issue><spage>266</spage><epage>272</epage><pages>266-272</pages><issn>1028-852X</issn><eissn>2008-823X</eissn><abstract>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.
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.
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.
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.</abstract><cop>Iran</cop><pub>Pasteur Institute of Iran</pub><pmid>27108691</pmid><doi>10.22045/ibj.2016.03</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Iranian biomedical journal, 2016-11, Vol.20 (5), p.266-272 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Connexins - metabolism Epilepsy Full Lenght Gap Junction delta-2 Protein Gap Junctions - drug effects Gap Junctions - metabolism Hippocampus - drug effects Hippocampus - physiopathology Histology Kindling, Neurologic - drug effects Male Quinine - pharmacology Rats Rats, Wistar Rodents Seizures - physiopathology Synaptic Transmission - drug effects Synaptic Transmission - physiology |
| title | Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions |
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