Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy
Peroxisomal proliferator-activated receptor gamma (PPARγ) is a nuclear hormone receptor whose agonist, rosiglitazone has a neuroprotective effect to hippocampal neurons in pilocarpine-induced seizures. Hippocampal slice preparations treated in Mg2+ free medium can induce ictal and interictal-like ep...
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| Veröffentlicht in: | PloS one 2015-12, Vol.10 (12), p.e0144806-e0144806 |
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| creator | Wong, Shi-Bing Cheng, Sin-Jhong Hung, Wei-Chen Lee, Wang-Tso Min, Ming-Yuan |
| description | Peroxisomal proliferator-activated receptor gamma (PPARγ) is a nuclear hormone receptor whose agonist, rosiglitazone has a neuroprotective effect to hippocampal neurons in pilocarpine-induced seizures. Hippocampal slice preparations treated in Mg2+ free medium can induce ictal and interictal-like epileptiform discharges, which is regarded as an in vitro model of N-methyl-D-aspartate (NMDA) receptor-mediated temporal lobe epilepsy (TLE). We applied rosiglitazone in hippocampal slices treated in Mg2+ free medium. The effects of rosiglitazone on hippocampal CA1-Schaffer collateral synaptic transmission were tested. We also examined the neuroprotective effect of rosiglitazone toward NMDA excitotoxicity on cultured hippocampal slices. Application of 10 μM rosiglitazone significantly suppressed amplitude and frequency of epileptiform discharges in CA1 neurons. Pretreatment with the PPARγ antagonist GW9662 did not block the effect of rosiglitazone on suppressing discharge frequency, but reverse the effect on suppressing discharge amplitude. Application of rosiglitazone suppressed synaptic transmission in the CA1-Schaffer collateral pathway. By miniature excitatory-potential synaptic current (mEPSC) analysis, rosiglitazone significantly suppressed presynaptic neurotransmitter release. This phenomenon can be reversed by pretreating PPARγ antagonist GW9662. Also, rosiglitazone protected cultured hippocampal slices from NMDA-induced excitotoxicity. The protective effect of 10 μM rosiglitazone was partially antagonized by concomitant high dose GW9662 treatment, indicating that this effect is partially mediated by PPARγ receptors. In conclusion, rosiglitazone suppressed NMDA receptor-mediated epileptiform discharges by inhibition of presynaptic neurotransmitter release. Rosiglitazone protected hippocampal slice from NMDA excitotoxicity partially by PPARγ activation. We suggest that rosiglitazone could be a potential agent to treat patients with TLE. |
| doi_str_mv | 10.1371/journal.pone.0144806 |
| format | Article |
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Hippocampal slice preparations treated in Mg2+ free medium can induce ictal and interictal-like epileptiform discharges, which is regarded as an in vitro model of N-methyl-D-aspartate (NMDA) receptor-mediated temporal lobe epilepsy (TLE). We applied rosiglitazone in hippocampal slices treated in Mg2+ free medium. The effects of rosiglitazone on hippocampal CA1-Schaffer collateral synaptic transmission were tested. We also examined the neuroprotective effect of rosiglitazone toward NMDA excitotoxicity on cultured hippocampal slices. Application of 10 μM rosiglitazone significantly suppressed amplitude and frequency of epileptiform discharges in CA1 neurons. Pretreatment with the PPARγ antagonist GW9662 did not block the effect of rosiglitazone on suppressing discharge frequency, but reverse the effect on suppressing discharge amplitude. Application of rosiglitazone suppressed synaptic transmission in the CA1-Schaffer collateral pathway. By miniature excitatory-potential synaptic current (mEPSC) analysis, rosiglitazone significantly suppressed presynaptic neurotransmitter release. This phenomenon can be reversed by pretreating PPARγ antagonist GW9662. Also, rosiglitazone protected cultured hippocampal slices from NMDA-induced excitotoxicity. The protective effect of 10 μM rosiglitazone was partially antagonized by concomitant high dose GW9662 treatment, indicating that this effect is partially mediated by PPARγ receptors. In conclusion, rosiglitazone suppressed NMDA receptor-mediated epileptiform discharges by inhibition of presynaptic neurotransmitter release. Rosiglitazone protected hippocampal slice from NMDA excitotoxicity partially by PPARγ activation. We suggest that rosiglitazone could be a potential agent to treat patients with TLE.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0144806</identifier><identifier>PMID: 26659605</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Action Potentials - drug effects ; Alzheimer's disease ; Anilides - pharmacology ; Animals ; Brain ; Brain slice preparation ; Buddhism ; CA1 Region, Hippocampal - drug effects ; CA1 Region, Hippocampal - metabolism ; CA1 Region, Hippocampal - pathology ; Culture Media - chemistry ; Culture Media - pharmacology ; Cytokines ; Discharge ; Discharge frequency ; Dosage and administration ; Drug therapy ; Drugs ; Epilepsy ; Epilepsy, Temporal Lobe - drug therapy ; Epilepsy, Temporal Lobe - genetics ; Epilepsy, Temporal Lobe - metabolism ; Epilepsy, Temporal Lobe - pathology ; Excitatory Postsynaptic Potentials - drug effects ; Excitotoxicity ; Firing pattern ; Gene expression ; Gene Expression Regulation ; Glucose ; Glutamate ; Glutamic Acid - metabolism ; Glutamic acid receptors (ionotropic) ; Health aspects ; Hippocampus ; Ischemia ; Kinases ; Life sciences ; Magnesium ; Magnesium - pharmacology ; Microtomy ; Models, Biological ; N-Methyl-D-aspartic acid receptors ; Neurons ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Neuroprotection ; Neuroprotective Agents - antagonists & inhibitors ; Neuroprotective Agents - pharmacology ; Neurotransmitter release ; Parkinson's disease ; Patient outcomes ; Pediatrics ; Pilocarpine ; PPAR gamma - antagonists & inhibitors ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Prevention ; Rats ; Rats, Sprague-Dawley ; Receptors ; Receptors, N-Methyl-D-Aspartate - agonists ; Receptors, N-Methyl-D-Aspartate - genetics ; Receptors, N-Methyl-D-Aspartate - metabolism ; Rodents ; Rosiglitazone ; Rosiglitazone maleate ; Seizures ; Seizures (Medicine) ; Seizures - drug therapy ; Seizures - genetics ; Seizures - metabolism ; Seizures - pathology ; Synapses ; Synaptic transmission ; Synaptic Transmission - drug effects ; Temporal lobe ; Thiazolidinediones - antagonists & inhibitors ; Thiazolidinediones - pharmacology ; Tissue Culture Techniques ; Zoology</subject><ispartof>PloS one, 2015-12, Vol.10 (12), p.e0144806-e0144806</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Wong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Wong et al 2015 Wong et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c622t-f7cd29880bce1d5d444a720ab15524752fa03bdd70ac03645b20b5321c009ddd3</citedby><cites>FETCH-LOGICAL-c622t-f7cd29880bce1d5d444a720ab15524752fa03bdd70ac03645b20b5321c009ddd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685987/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685987/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26659605$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Brown, Jon</contributor><creatorcontrib>Wong, Shi-Bing</creatorcontrib><creatorcontrib>Cheng, Sin-Jhong</creatorcontrib><creatorcontrib>Hung, Wei-Chen</creatorcontrib><creatorcontrib>Lee, Wang-Tso</creatorcontrib><creatorcontrib>Min, Ming-Yuan</creatorcontrib><title>Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Peroxisomal proliferator-activated receptor gamma (PPARγ) is a nuclear hormone receptor whose agonist, rosiglitazone has a neuroprotective effect to hippocampal neurons in pilocarpine-induced seizures. Hippocampal slice preparations treated in Mg2+ free medium can induce ictal and interictal-like epileptiform discharges, which is regarded as an in vitro model of N-methyl-D-aspartate (NMDA) receptor-mediated temporal lobe epilepsy (TLE). We applied rosiglitazone in hippocampal slices treated in Mg2+ free medium. The effects of rosiglitazone on hippocampal CA1-Schaffer collateral synaptic transmission were tested. We also examined the neuroprotective effect of rosiglitazone toward NMDA excitotoxicity on cultured hippocampal slices. Application of 10 μM rosiglitazone significantly suppressed amplitude and frequency of epileptiform discharges in CA1 neurons. Pretreatment with the PPARγ antagonist GW9662 did not block the effect of rosiglitazone on suppressing discharge frequency, but reverse the effect on suppressing discharge amplitude. Application of rosiglitazone suppressed synaptic transmission in the CA1-Schaffer collateral pathway. By miniature excitatory-potential synaptic current (mEPSC) analysis, rosiglitazone significantly suppressed presynaptic neurotransmitter release. This phenomenon can be reversed by pretreating PPARγ antagonist GW9662. Also, rosiglitazone protected cultured hippocampal slices from NMDA-induced excitotoxicity. The protective effect of 10 μM rosiglitazone was partially antagonized by concomitant high dose GW9662 treatment, indicating that this effect is partially mediated by PPARγ receptors. In conclusion, rosiglitazone suppressed NMDA receptor-mediated epileptiform discharges by inhibition of presynaptic neurotransmitter release. Rosiglitazone protected hippocampal slice from NMDA excitotoxicity partially by PPARγ activation. We suggest that rosiglitazone could be a potential agent to treat patients with TLE.</description><subject>Action Potentials - drug effects</subject><subject>Alzheimer's disease</subject><subject>Anilides - pharmacology</subject><subject>Animals</subject><subject>Brain</subject><subject>Brain slice preparation</subject><subject>Buddhism</subject><subject>CA1 Region, Hippocampal - drug effects</subject><subject>CA1 Region, Hippocampal - metabolism</subject><subject>CA1 Region, Hippocampal - pathology</subject><subject>Culture Media - chemistry</subject><subject>Culture Media - pharmacology</subject><subject>Cytokines</subject><subject>Discharge</subject><subject>Discharge frequency</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Drugs</subject><subject>Epilepsy</subject><subject>Epilepsy, Temporal Lobe - drug therapy</subject><subject>Epilepsy, Temporal Lobe - genetics</subject><subject>Epilepsy, Temporal Lobe - metabolism</subject><subject>Epilepsy, Temporal Lobe - pathology</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Excitotoxicity</subject><subject>Firing pattern</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Glucose</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Health aspects</subject><subject>Hippocampus</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Life sciences</subject><subject>Magnesium</subject><subject>Magnesium - pharmacology</subject><subject>Microtomy</subject><subject>Models, Biological</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - antagonists & inhibitors</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neurotransmitter release</subject><subject>Parkinson's disease</subject><subject>Patient outcomes</subject><subject>Pediatrics</subject><subject>Pilocarpine</subject><subject>PPAR gamma - antagonists & inhibitors</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Prevention</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors</subject><subject>Receptors, N-Methyl-D-Aspartate - agonists</subject><subject>Receptors, N-Methyl-D-Aspartate - genetics</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Rodents</subject><subject>Rosiglitazone</subject><subject>Rosiglitazone maleate</subject><subject>Seizures</subject><subject>Seizures (Medicine)</subject><subject>Seizures - drug therapy</subject><subject>Seizures - genetics</subject><subject>Seizures - metabolism</subject><subject>Seizures - pathology</subject><subject>Synapses</subject><subject>Synaptic transmission</subject><subject>Synaptic Transmission - drug effects</subject><subject>Temporal lobe</subject><subject>Thiazolidinediones - antagonists & inhibitors</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Tissue Culture Techniques</subject><subject>Zoology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk91u0zAUxyMEYmPwBggsISG4aLET20lukKZpbJWKhtqxW-vEPmk9OXGIE0T3FDwyLuumFe0C-cKW_Tv_4_OVJK8ZnbIsZ5-u_di34Kadb3FKGecFlU-SQ1Zm6USmNHv64HyQvAjhmlKRFVI-Tw5SKUUpqThMfi98sCtnB7iJOmQ5dl2PIWAgs5Zc2aH3ZIn2ZoyXxLbk3Had19B04MjSWY2k2kRybSs72HZFvkVu00I3WE3O3DhAAwOSBTqEgFsBIF-9QUd8TS6x6Xwfhea-QnLaWYdd2LxMntXgAr7a7UfJ9y-nlyfnk_nF2ezkeD7RMk2HSZ1rk5ZFQSuNzAjDOYc8pVAxIVKei7QGmlXG5BQ0zSQXVUorkaVMU1oaY7Kj5O2tbud8ULtkBsVyXhSSS5ZHYnZLGA_XquttA_1GebDq74XvVwr6GKhDRcuq0JyLknHNGZgCy6rMM5aLGkwOOmp93nkbqwaNxnaIke-J7r-0dq1W_qfishBlsf3Mh51A73-MGAbV2KDROWjRj9t_C0opSyWN6Lt_0Mej21EriAHYtvbRr96KqmOe5VxKxkSkpo9QcRlsrI4dU8eq7Rt83DOIzIC_hhWMIajZcvH_7MXVPvv-AbtGcMM6-Nhh1rdhH-S3oO59CD3W90lmVG0H5y4bajs4ajc40ezNwwLdG91NSvYHCJ0Uag</recordid><startdate>20151214</startdate><enddate>20151214</enddate><creator>Wong, Shi-Bing</creator><creator>Cheng, Sin-Jhong</creator><creator>Hung, Wei-Chen</creator><creator>Lee, Wang-Tso</creator><creator>Min, Ming-Yuan</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20151214</creationdate><title>Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy</title><author>Wong, Shi-Bing ; Cheng, Sin-Jhong ; Hung, Wei-Chen ; Lee, Wang-Tso ; Min, Ming-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c622t-f7cd29880bce1d5d444a720ab15524752fa03bdd70ac03645b20b5321c009ddd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Action Potentials - drug effects</topic><topic>Alzheimer's disease</topic><topic>Anilides - pharmacology</topic><topic>Animals</topic><topic>Brain</topic><topic>Brain slice preparation</topic><topic>Buddhism</topic><topic>CA1 Region, Hippocampal - drug effects</topic><topic>CA1 Region, Hippocampal - metabolism</topic><topic>CA1 Region, Hippocampal - pathology</topic><topic>Culture Media - chemistry</topic><topic>Culture Media - pharmacology</topic><topic>Cytokines</topic><topic>Discharge</topic><topic>Discharge frequency</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Drugs</topic><topic>Epilepsy</topic><topic>Epilepsy, Temporal Lobe - drug therapy</topic><topic>Epilepsy, Temporal Lobe - genetics</topic><topic>Epilepsy, Temporal Lobe - metabolism</topic><topic>Epilepsy, Temporal Lobe - pathology</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Excitotoxicity</topic><topic>Firing pattern</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Glucose</topic><topic>Glutamate</topic><topic>Glutamic Acid - metabolism</topic><topic>Glutamic acid receptors (ionotropic)</topic><topic>Health aspects</topic><topic>Hippocampus</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Life sciences</topic><topic>Magnesium</topic><topic>Magnesium - pharmacology</topic><topic>Microtomy</topic><topic>Models, Biological</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - antagonists & inhibitors</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neurotransmitter release</topic><topic>Parkinson's disease</topic><topic>Patient outcomes</topic><topic>Pediatrics</topic><topic>Pilocarpine</topic><topic>PPAR gamma - antagonists & inhibitors</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Prevention</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors</topic><topic>Receptors, N-Methyl-D-Aspartate - agonists</topic><topic>Receptors, N-Methyl-D-Aspartate - genetics</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Rodents</topic><topic>Rosiglitazone</topic><topic>Rosiglitazone maleate</topic><topic>Seizures</topic><topic>Seizures (Medicine)</topic><topic>Seizures - drug therapy</topic><topic>Seizures - genetics</topic><topic>Seizures - metabolism</topic><topic>Seizures - pathology</topic><topic>Synapses</topic><topic>Synaptic transmission</topic><topic>Synaptic Transmission - drug effects</topic><topic>Temporal lobe</topic><topic>Thiazolidinediones - antagonists & inhibitors</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Tissue Culture Techniques</topic><topic>Zoology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wong, Shi-Bing</creatorcontrib><creatorcontrib>Cheng, Sin-Jhong</creatorcontrib><creatorcontrib>Hung, Wei-Chen</creatorcontrib><creatorcontrib>Lee, Wang-Tso</creatorcontrib><creatorcontrib>Min, Ming-Yuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wong, Shi-Bing</au><au>Cheng, Sin-Jhong</au><au>Hung, Wei-Chen</au><au>Lee, Wang-Tso</au><au>Min, Ming-Yuan</au><au>Brown, Jon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-12-14</date><risdate>2015</risdate><volume>10</volume><issue>12</issue><spage>e0144806</spage><epage>e0144806</epage><pages>e0144806-e0144806</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Peroxisomal proliferator-activated receptor gamma (PPARγ) is a nuclear hormone receptor whose agonist, rosiglitazone has a neuroprotective effect to hippocampal neurons in pilocarpine-induced seizures. Hippocampal slice preparations treated in Mg2+ free medium can induce ictal and interictal-like epileptiform discharges, which is regarded as an in vitro model of N-methyl-D-aspartate (NMDA) receptor-mediated temporal lobe epilepsy (TLE). We applied rosiglitazone in hippocampal slices treated in Mg2+ free medium. The effects of rosiglitazone on hippocampal CA1-Schaffer collateral synaptic transmission were tested. We also examined the neuroprotective effect of rosiglitazone toward NMDA excitotoxicity on cultured hippocampal slices. Application of 10 μM rosiglitazone significantly suppressed amplitude and frequency of epileptiform discharges in CA1 neurons. Pretreatment with the PPARγ antagonist GW9662 did not block the effect of rosiglitazone on suppressing discharge frequency, but reverse the effect on suppressing discharge amplitude. Application of rosiglitazone suppressed synaptic transmission in the CA1-Schaffer collateral pathway. By miniature excitatory-potential synaptic current (mEPSC) analysis, rosiglitazone significantly suppressed presynaptic neurotransmitter release. This phenomenon can be reversed by pretreating PPARγ antagonist GW9662. Also, rosiglitazone protected cultured hippocampal slices from NMDA-induced excitotoxicity. The protective effect of 10 μM rosiglitazone was partially antagonized by concomitant high dose GW9662 treatment, indicating that this effect is partially mediated by PPARγ receptors. In conclusion, rosiglitazone suppressed NMDA receptor-mediated epileptiform discharges by inhibition of presynaptic neurotransmitter release. Rosiglitazone protected hippocampal slice from NMDA excitotoxicity partially by PPARγ activation. We suggest that rosiglitazone could be a potential agent to treat patients with TLE.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26659605</pmid><doi>10.1371/journal.pone.0144806</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-12, Vol.10 (12), p.e0144806-e0144806 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1748864617 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Action Potentials - drug effects Alzheimer's disease Anilides - pharmacology Animals Brain Brain slice preparation Buddhism CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - metabolism CA1 Region, Hippocampal - pathology Culture Media - chemistry Culture Media - pharmacology Cytokines Discharge Discharge frequency Dosage and administration Drug therapy Drugs Epilepsy Epilepsy, Temporal Lobe - drug therapy Epilepsy, Temporal Lobe - genetics Epilepsy, Temporal Lobe - metabolism Epilepsy, Temporal Lobe - pathology Excitatory Postsynaptic Potentials - drug effects Excitotoxicity Firing pattern Gene expression Gene Expression Regulation Glucose Glutamate Glutamic Acid - metabolism Glutamic acid receptors (ionotropic) Health aspects Hippocampus Ischemia Kinases Life sciences Magnesium Magnesium - pharmacology Microtomy Models, Biological N-Methyl-D-aspartic acid receptors Neurons Neurons - drug effects Neurons - metabolism Neurons - pathology Neuroprotection Neuroprotective Agents - antagonists & inhibitors Neuroprotective Agents - pharmacology Neurotransmitter release Parkinson's disease Patient outcomes Pediatrics Pilocarpine PPAR gamma - antagonists & inhibitors PPAR gamma - genetics PPAR gamma - metabolism Prevention Rats Rats, Sprague-Dawley Receptors Receptors, N-Methyl-D-Aspartate - agonists Receptors, N-Methyl-D-Aspartate - genetics Receptors, N-Methyl-D-Aspartate - metabolism Rodents Rosiglitazone Rosiglitazone maleate Seizures Seizures (Medicine) Seizures - drug therapy Seizures - genetics Seizures - metabolism Seizures - pathology Synapses Synaptic transmission Synaptic Transmission - drug effects Temporal lobe Thiazolidinediones - antagonists & inhibitors Thiazolidinediones - pharmacology Tissue Culture Techniques Zoology |
| title | Rosiglitazone Suppresses In Vitro Seizures in Hippocampal Slice by Inhibiting Presynaptic Glutamate Release in a Model of Temporal Lobe Epilepsy |
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