Hippocampal Programmed Cell Death after Status Epilepticus
Summary: Purpose: Status epilepticus (SE) can result in acute neuronal injury with subsequent long-term age-dependent behavioral and histologic sequelae. To investigate potential mechanisms that may underlie SE-related neuronal injury, we studied the occurrence of programmed cell death (PCD) in the...
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2003
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| Online Access: | http://hdl.handle.net/10725/2734 http://dx.doi.org/10.1046/j.1528-1157.2003.22502.x http://onlinelibrary.wiley.com/doi/10.1046/j.1528-1157.2003.22502.x/full |
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| _version_ | 1864513459122601984 |
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| author | Abi-Habib, Ralph J. |
| author2 | Kobbeissi, Mohamad Farhat, Firas Dbaibo, Ghassan S. Kurdi, Rana M. Mikati, Mohamad A. El Sabban, Marwan E. Asaad, Wissal |
| author2_role | author author author author author author author |
| author_facet | Abi-Habib, Ralph J. Kobbeissi, Mohamad Farhat, Firas Dbaibo, Ghassan S. Kurdi, Rana M. Mikati, Mohamad A. El Sabban, Marwan E. Asaad, Wissal |
| author_role | author |
| dc.creator.none.fl_str_mv | Abi-Habib, Ralph J. Kobbeissi, Mohamad Farhat, Firas Dbaibo, Ghassan S. Kurdi, Rana M. Mikati, Mohamad A. El Sabban, Marwan E. Asaad, Wissal |
| dc.date.none.fl_str_mv | 2003 2015-11-30T09:46:42Z 2015-11-30T09:46:42Z 2015-11-30 |
| dc.identifier.none.fl_str_mv | 0013-9580 http://hdl.handle.net/10725/2734 http://dx.doi.org/10.1046/j.1528-1157.2003.22502.x Mikati, M. A., Abi‐Habib, R. J., El Sabban, M. E., Dbaibo, G. S., Kurdi, R. M., Kobeissi, M., ... & Asaad, W. (2003). Hippocampal Programmed Cell Death after Status Epilepticus: Evidence for NMDA‐Receptor and Ceramide‐Mediated Mechanisms. Epilepsia, 44(3), 282-291. http://onlinelibrary.wiley.com/doi/10.1046/j.1528-1157.2003.22502.x/full |
| dc.language.none.fl_str_mv | en |
| dc.relation.none.fl_str_mv | Epilepsia |
| dc.rights.*.fl_str_mv | info:eu-repo/semantics/openAccess |
| dc.title.none.fl_str_mv | Hippocampal Programmed Cell Death after Status Epilepticus Evidence for NMDA-Receptor and Ceramide-Mediated Mechanisms |
| dc.type.none.fl_str_mv | Article info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/article |
| description | Summary: Purpose: Status epilepticus (SE) can result in acute neuronal injury with subsequent long-term age-dependent behavioral and histologic sequelae. To investigate potential mechanisms that may underlie SE-related neuronal injury, we studied the occurrence of programmed cell death (PCD) in the hippocampus in the kainic acid (KA) model. Methods: In adult rats, KA-induced SE resulted in DNA fragmentation documented at 30 h after KA injection. Ceramide, a known mediator of PCD in multiple neural and nonneural tissues, increased at 2–3 h after KA intraperitoneal injection, and then decreased to control levels before increasing again from 12 to 30 h after injection. MK801 pretreatment prevented KA-induced increases in ceramide levels and DNA fragmentation, whether there was reduction in seizure severity or not (achieved with 5 mg/kg and 1 mg/kg of MK801, respectively). Results: Both ceramide increases and DNA fragmentation were observed after KA-induced SE in adult and in P35 rats. Ceramide did not increase after KA-induced SE in P7 pups, which also did not manifest any DNA fragmentation. Intrahippocampal injection of the active ceramide analogue C2-ceramide produced widespread DNA fragmentation, whereas the inactive ceramide analogue C2-dihydroceramide did not. Conclusions: Our data support the hypotheses that (a) N-methyl-d-aspartate–receptor activation results in ceramide increases and in DNA fragmentation; (b) ceramide is a mediator of PCD after SE; and (c) there are age-related differences in PCD and in the ceramide response after SE. Differences in the ceramide response could, potentially, be responsible for observed age-related differences in the response to SE. |
| eu_rights_str_mv | openAccess |
| format | article |
| id | LAURepo_bdde51c4e6b294696190b723cc267ff2 |
| identifier_str_mv | 0013-9580 Mikati, M. A., Abi‐Habib, R. J., El Sabban, M. E., Dbaibo, G. S., Kurdi, R. M., Kobeissi, M., ... & Asaad, W. (2003). Hippocampal Programmed Cell Death after Status Epilepticus: Evidence for NMDA‐Receptor and Ceramide‐Mediated Mechanisms. Epilepsia, 44(3), 282-291. |
| language_invalid_str_mv | en |
| network_acronym_str | LAURepo |
| network_name_str | Lebanese American University repository |
| oai_identifier_str | oai:laur.lau.edu.lb:10725/2734 |
| publishDate | 2003 |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| spelling | Hippocampal Programmed Cell Death after Status EpilepticusEvidence for NMDA-Receptor and Ceramide-Mediated MechanismsAbi-Habib, Ralph J.Kobbeissi, MohamadFarhat, FirasDbaibo, Ghassan S.Kurdi, Rana M.Mikati, Mohamad A.El Sabban, Marwan E.Asaad, WissalSummary: Purpose: Status epilepticus (SE) can result in acute neuronal injury with subsequent long-term age-dependent behavioral and histologic sequelae. To investigate potential mechanisms that may underlie SE-related neuronal injury, we studied the occurrence of programmed cell death (PCD) in the hippocampus in the kainic acid (KA) model. Methods: In adult rats, KA-induced SE resulted in DNA fragmentation documented at 30 h after KA injection. Ceramide, a known mediator of PCD in multiple neural and nonneural tissues, increased at 2–3 h after KA intraperitoneal injection, and then decreased to control levels before increasing again from 12 to 30 h after injection. MK801 pretreatment prevented KA-induced increases in ceramide levels and DNA fragmentation, whether there was reduction in seizure severity or not (achieved with 5 mg/kg and 1 mg/kg of MK801, respectively). Results: Both ceramide increases and DNA fragmentation were observed after KA-induced SE in adult and in P35 rats. Ceramide did not increase after KA-induced SE in P7 pups, which also did not manifest any DNA fragmentation. Intrahippocampal injection of the active ceramide analogue C2-ceramide produced widespread DNA fragmentation, whereas the inactive ceramide analogue C2-dihydroceramide did not. Conclusions: Our data support the hypotheses that (a) N-methyl-d-aspartate–receptor activation results in ceramide increases and in DNA fragmentation; (b) ceramide is a mediator of PCD after SE; and (c) there are age-related differences in PCD and in the ceramide response after SE. Differences in the ceramide response could, potentially, be responsible for observed age-related differences in the response to SE.PublishedN/A2015-11-30T09:46:42Z2015-11-30T09:46:42Z20032015-11-30Articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article0013-9580http://hdl.handle.net/10725/2734http://dx.doi.org/10.1046/j.1528-1157.2003.22502.xMikati, M. A., Abi‐Habib, R. J., El Sabban, M. E., Dbaibo, G. S., Kurdi, R. M., Kobeissi, M., ... & Asaad, W. (2003). Hippocampal Programmed Cell Death after Status Epilepticus: Evidence for NMDA‐Receptor and Ceramide‐Mediated Mechanisms. Epilepsia, 44(3), 282-291.http://onlinelibrary.wiley.com/doi/10.1046/j.1528-1157.2003.22502.x/fullenEpilepsiainfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/27342016-08-26T09:30:01Z |
| spellingShingle | Hippocampal Programmed Cell Death after Status Epilepticus Abi-Habib, Ralph J. |
| status_str | publishedVersion |
| title | Hippocampal Programmed Cell Death after Status Epilepticus |
| title_full | Hippocampal Programmed Cell Death after Status Epilepticus |
| title_fullStr | Hippocampal Programmed Cell Death after Status Epilepticus |
| title_full_unstemmed | Hippocampal Programmed Cell Death after Status Epilepticus |
| title_short | Hippocampal Programmed Cell Death after Status Epilepticus |
| title_sort | Hippocampal Programmed Cell Death after Status Epilepticus |
| url | http://hdl.handle.net/10725/2734 http://dx.doi.org/10.1046/j.1528-1157.2003.22502.x http://onlinelibrary.wiley.com/doi/10.1046/j.1528-1157.2003.22502.x/full |