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Dopaminergic modulation of low-Mg2+-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro
To investigate whether epileptiform activity in the immature brain is modulated by dopamine, we examined the effects of dopaminergic agonists and antagonists in an intact in vitro preparation of the isolated corticohippocampal formation of immature (postnatal days 3 and 4) C57/Bl6 mice using field p...
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| Published in: | Journal of neuroscience research 2012-10, Vol.90 (10), p.2020-2033 |
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| container_end_page | 2033 |
| container_issue | 10 |
| container_start_page | 2020 |
| container_title | Journal of neuroscience research |
| container_volume | 90 |
| creator | Sharopov, Salim Moser, Jochen Chen, Rongqing Kolbaev, Sergey N. Bernedo, Viviane E. Werhahn, Konrad J. Luhmann, Heiko J. Kilb, Werner |
| description | To investigate whether epileptiform activity in the immature brain is modulated by dopamine, we examined the effects of dopaminergic agonists and antagonists in an intact in vitro preparation of the isolated corticohippocampal formation of immature (postnatal days 3 and 4) C57/Bl6 mice using field potential recordings from CA3. Epileptiform discharges were induced by a reduction of the extracellular Mg2+ concentration to 0.2 mM. These experiments revealed that low concentrations of dopamine (3 μM dopamine enhanced epileptiform activity. The D1‐agonist SKF38393 (10 μM) had a strong proconvulsive effect, and the D2‐like agonist quinpirole (10 μM) mediated a weak anticonvulsive effect. The proconvulsive effect of 10 μM dopamine was completely abolished by the D1‐like receptor antagonist SCH39166 (2 μM) or the D2‐like antagonist sulpiride (10 μM), whereas the D2 antagonist L‐741626 (50 nM) and the D3 antagonist SB‐277011‐A (0.1 μM) were without effect. The anticonvulsive effect of 0.1 μM dopamine could be suppressed by D1‐like, D2, or D3 receptor antagonists. A proconvulsive effect of 10 μM dopamine was also observed when AMPA, NMDA, or GABAA receptors were blocked. In summary, these results suggest that 1) dopamine influences epileptiform activity already at early developmental stages; 2) dopamine can bidirectionally influence the excitability; 3) D1‐like receptors mediate the proconvulsive effect of high dopamine concentrations, although the pharmacology of the anticonvulsive effect is less clear; and 4) dopamine‐induced alterations in GABAergic and glutamatergic systems may contribute to this effect. © 2012 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jnr.23084 |
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Epileptiform discharges were induced by a reduction of the extracellular Mg2+ concentration to 0.2 mM. These experiments revealed that low concentrations of dopamine (<0.3 μM) attenuated epileptiform activity, whereas >3 μM dopamine enhanced epileptiform activity. The D1‐agonist SKF38393 (10 μM) had a strong proconvulsive effect, and the D2‐like agonist quinpirole (10 μM) mediated a weak anticonvulsive effect. The proconvulsive effect of 10 μM dopamine was completely abolished by the D1‐like receptor antagonist SCH39166 (2 μM) or the D2‐like antagonist sulpiride (10 μM), whereas the D2 antagonist L‐741626 (50 nM) and the D3 antagonist SB‐277011‐A (0.1 μM) were without effect. The anticonvulsive effect of 0.1 μM dopamine could be suppressed by D1‐like, D2, or D3 receptor antagonists. A proconvulsive effect of 10 μM dopamine was also observed when AMPA, NMDA, or GABAA receptors were blocked. In summary, these results suggest that 1) dopamine influences epileptiform activity already at early developmental stages; 2) dopamine can bidirectionally influence the excitability; 3) D1‐like receptors mediate the proconvulsive effect of high dopamine concentrations, although the pharmacology of the anticonvulsive effect is less clear; and 4) dopamine‐induced alterations in GABAergic and glutamatergic systems may contribute to this effect. © 2012 Wiley Periodicals, Inc.</description><identifier>ISSN: 0360-4012</identifier><identifier>EISSN: 1097-4547</identifier><identifier>DOI: 10.1002/jnr.23084</identifier><identifier>PMID: 22714119</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology ; Animals ; Animals, Newborn ; Benzazepines - pharmacology ; Data Interpretation, Statistical ; development ; Dopamine - pharmacology ; Dopamine - physiology ; Dopamine Agonists - pharmacology ; Dopamine Antagonists - pharmacology ; Dopamine D2 Receptor Antagonists ; dopamine receptor ; epilepsy ; Epilepsy - physiopathology ; Hippocampus - physiopathology ; Indoles - pharmacology ; Magnesium Deficiency - physiopathology ; Mice ; Mice, Inbred C57BL ; Nitriles - pharmacology ; Piperidines - pharmacology ; Quinpirole - pharmacology ; Receptors, Dopamine D2 - agonists ; seizures ; Synapses - drug effects ; Tetrahydroisoquinolines - pharmacology</subject><ispartof>Journal of neuroscience research, 2012-10, Vol.90 (10), p.2020-2033</ispartof><rights>Copyright © 2012 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjnr.23084$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjnr.23084$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22714119$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sharopov, Salim</creatorcontrib><creatorcontrib>Moser, Jochen</creatorcontrib><creatorcontrib>Chen, Rongqing</creatorcontrib><creatorcontrib>Kolbaev, Sergey N.</creatorcontrib><creatorcontrib>Bernedo, Viviane E.</creatorcontrib><creatorcontrib>Werhahn, Konrad J.</creatorcontrib><creatorcontrib>Luhmann, Heiko J.</creatorcontrib><creatorcontrib>Kilb, Werner</creatorcontrib><title>Dopaminergic modulation of low-Mg2+-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro</title><title>Journal of neuroscience research</title><addtitle>J. Neurosci. Res</addtitle><description>To investigate whether epileptiform activity in the immature brain is modulated by dopamine, we examined the effects of dopaminergic agonists and antagonists in an intact in vitro preparation of the isolated corticohippocampal formation of immature (postnatal days 3 and 4) C57/Bl6 mice using field potential recordings from CA3. Epileptiform discharges were induced by a reduction of the extracellular Mg2+ concentration to 0.2 mM. These experiments revealed that low concentrations of dopamine (<0.3 μM) attenuated epileptiform activity, whereas >3 μM dopamine enhanced epileptiform activity. The D1‐agonist SKF38393 (10 μM) had a strong proconvulsive effect, and the D2‐like agonist quinpirole (10 μM) mediated a weak anticonvulsive effect. The proconvulsive effect of 10 μM dopamine was completely abolished by the D1‐like receptor antagonist SCH39166 (2 μM) or the D2‐like antagonist sulpiride (10 μM), whereas the D2 antagonist L‐741626 (50 nM) and the D3 antagonist SB‐277011‐A (0.1 μM) were without effect. The anticonvulsive effect of 0.1 μM dopamine could be suppressed by D1‐like, D2, or D3 receptor antagonists. A proconvulsive effect of 10 μM dopamine was also observed when AMPA, NMDA, or GABAA receptors were blocked. In summary, these results suggest that 1) dopamine influences epileptiform activity already at early developmental stages; 2) dopamine can bidirectionally influence the excitability; 3) D1‐like receptors mediate the proconvulsive effect of high dopamine concentrations, although the pharmacology of the anticonvulsive effect is less clear; and 4) dopamine‐induced alterations in GABAergic and glutamatergic systems may contribute to this effect. © 2012 Wiley Periodicals, Inc.</description><subject>2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Benzazepines - pharmacology</subject><subject>Data Interpretation, Statistical</subject><subject>development</subject><subject>Dopamine - pharmacology</subject><subject>Dopamine - physiology</subject><subject>Dopamine Agonists - pharmacology</subject><subject>Dopamine Antagonists - pharmacology</subject><subject>Dopamine D2 Receptor Antagonists</subject><subject>dopamine receptor</subject><subject>epilepsy</subject><subject>Epilepsy - physiopathology</subject><subject>Hippocampus - physiopathology</subject><subject>Indoles - pharmacology</subject><subject>Magnesium Deficiency - physiopathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nitriles - pharmacology</subject><subject>Piperidines - pharmacology</subject><subject>Quinpirole - pharmacology</subject><subject>Receptors, Dopamine D2 - agonists</subject><subject>seizures</subject><subject>Synapses - drug effects</subject><subject>Tetrahydroisoquinolines - pharmacology</subject><issn>0360-4012</issn><issn>1097-4547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNo9kV1PwjAUhhujEfy48A-YXpqYQb-2rpcGBSWIidFw2XRbB8Vtnd0m8u8tgt6cc9LzvG-a8wJwhdEAI0SG68oNCEUxOwJ9jAQPWMj4MegjGqGAIUx64Kxp1gghIUJ6CnqEcMwwFn2wvbe1Kk2l3dKksLRZV6jW2AraHBZ2EzwvyW1gqqxLdQZ1bQpdtya3roQqbc2XabfQVLBdad9a_wRXpq5tqsq6a3Yeu02lN4l1lXfvmh0HvczZC3CSq6LRl4d-Dt7HD2-jx2D2Mnka3c0CQ7BgAeWc6izSPEuIiGhM0zxOc0HChCc8UkyFNArjmKRMYF-wjpEiROAojuKchBk9Bzd739rZz043rSxNk-qiUJX2H5IYUcpCwoTw6PUB7ZJSZ7J2plRuK__O5YHhHtj4Q2z_9xjJXQ7S5yB_c5DT-evv4BXBXmGaVn__K5T7kBGnPJSL-UTiVzoeT-cLKegPiC-KDQ</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Sharopov, Salim</creator><creator>Moser, Jochen</creator><creator>Chen, Rongqing</creator><creator>Kolbaev, Sergey N.</creator><creator>Bernedo, Viviane E.</creator><creator>Werhahn, Konrad J.</creator><creator>Luhmann, Heiko J.</creator><creator>Kilb, Werner</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201210</creationdate><title>Dopaminergic modulation of low-Mg2+-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro</title><author>Sharopov, Salim ; Moser, Jochen ; Chen, Rongqing ; Kolbaev, Sergey N. ; Bernedo, Viviane E. ; Werhahn, Konrad J. ; Luhmann, Heiko J. ; Kilb, Werner</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2194-3773ed6e7db296383cf8cf925b7b76a4a5365882c4912c41e80a22916868f25d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Benzazepines - pharmacology</topic><topic>Data Interpretation, Statistical</topic><topic>development</topic><topic>Dopamine - pharmacology</topic><topic>Dopamine - physiology</topic><topic>Dopamine Agonists - pharmacology</topic><topic>Dopamine Antagonists - pharmacology</topic><topic>Dopamine D2 Receptor Antagonists</topic><topic>dopamine receptor</topic><topic>epilepsy</topic><topic>Epilepsy - physiopathology</topic><topic>Hippocampus - physiopathology</topic><topic>Indoles - pharmacology</topic><topic>Magnesium Deficiency - physiopathology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Nitriles - pharmacology</topic><topic>Piperidines - pharmacology</topic><topic>Quinpirole - pharmacology</topic><topic>Receptors, Dopamine D2 - agonists</topic><topic>seizures</topic><topic>Synapses - drug effects</topic><topic>Tetrahydroisoquinolines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sharopov, Salim</creatorcontrib><creatorcontrib>Moser, Jochen</creatorcontrib><creatorcontrib>Chen, Rongqing</creatorcontrib><creatorcontrib>Kolbaev, Sergey N.</creatorcontrib><creatorcontrib>Bernedo, Viviane E.</creatorcontrib><creatorcontrib>Werhahn, Konrad J.</creatorcontrib><creatorcontrib>Luhmann, Heiko J.</creatorcontrib><creatorcontrib>Kilb, Werner</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sharopov, Salim</au><au>Moser, Jochen</au><au>Chen, Rongqing</au><au>Kolbaev, Sergey N.</au><au>Bernedo, Viviane E.</au><au>Werhahn, Konrad J.</au><au>Luhmann, Heiko J.</au><au>Kilb, Werner</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dopaminergic modulation of low-Mg2+-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro</atitle><jtitle>Journal of neuroscience research</jtitle><addtitle>J. Neurosci. Res</addtitle><date>2012-10</date><risdate>2012</risdate><volume>90</volume><issue>10</issue><spage>2020</spage><epage>2033</epage><pages>2020-2033</pages><issn>0360-4012</issn><eissn>1097-4547</eissn><notes>istex:072619F2998730A7804469A50261DB55ABE2C634</notes><notes>ArticleID:JNR23084</notes><notes>DFG</notes><notes>ark:/67375/WNG-1R3FFJNW-9</notes><notes>MAIFOR program of the University of Medicine Mainz</notes><notes>H.W. and J. Hector Stiftung - No. M46</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>To investigate whether epileptiform activity in the immature brain is modulated by dopamine, we examined the effects of dopaminergic agonists and antagonists in an intact in vitro preparation of the isolated corticohippocampal formation of immature (postnatal days 3 and 4) C57/Bl6 mice using field potential recordings from CA3. Epileptiform discharges were induced by a reduction of the extracellular Mg2+ concentration to 0.2 mM. These experiments revealed that low concentrations of dopamine (<0.3 μM) attenuated epileptiform activity, whereas >3 μM dopamine enhanced epileptiform activity. The D1‐agonist SKF38393 (10 μM) had a strong proconvulsive effect, and the D2‐like agonist quinpirole (10 μM) mediated a weak anticonvulsive effect. The proconvulsive effect of 10 μM dopamine was completely abolished by the D1‐like receptor antagonist SCH39166 (2 μM) or the D2‐like antagonist sulpiride (10 μM), whereas the D2 antagonist L‐741626 (50 nM) and the D3 antagonist SB‐277011‐A (0.1 μM) were without effect. The anticonvulsive effect of 0.1 μM dopamine could be suppressed by D1‐like, D2, or D3 receptor antagonists. A proconvulsive effect of 10 μM dopamine was also observed when AMPA, NMDA, or GABAA receptors were blocked. In summary, these results suggest that 1) dopamine influences epileptiform activity already at early developmental stages; 2) dopamine can bidirectionally influence the excitability; 3) D1‐like receptors mediate the proconvulsive effect of high dopamine concentrations, although the pharmacology of the anticonvulsive effect is less clear; and 4) dopamine‐induced alterations in GABAergic and glutamatergic systems may contribute to this effect. © 2012 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22714119</pmid><doi>10.1002/jnr.23084</doi><tpages>14</tpages></addata></record> |
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| subjects | 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology Animals Animals, Newborn Benzazepines - pharmacology Data Interpretation, Statistical development Dopamine - pharmacology Dopamine - physiology Dopamine Agonists - pharmacology Dopamine Antagonists - pharmacology Dopamine D2 Receptor Antagonists dopamine receptor epilepsy Epilepsy - physiopathology Hippocampus - physiopathology Indoles - pharmacology Magnesium Deficiency - physiopathology Mice Mice, Inbred C57BL Nitriles - pharmacology Piperidines - pharmacology Quinpirole - pharmacology Receptors, Dopamine D2 - agonists seizures Synapses - drug effects Tetrahydroisoquinolines - pharmacology |
| title | Dopaminergic modulation of low-Mg2+-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro |
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