Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats
Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion corti...
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MDPI AG
2021-05-01
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| Series: | International Journal of Molecular Sciences |
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| author | Ilia G. Komoltsev Stepan O. Frankevich Natalia I. Shirobokova Aleksandra A. Volkova Mikhail V. Onufriev Julia V. Moiseeva Margarita R. Novikova Natalia V. Gulyaeva |
| author_facet | Ilia G. Komoltsev Stepan O. Frankevich Natalia I. Shirobokova Aleksandra A. Volkova Mikhail V. Onufriev Julia V. Moiseeva Margarita R. Novikova Natalia V. Gulyaeva |
| author_sort | Ilia G. Komoltsev |
| collection | DOAJ |
| description | Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), we assessed potential association of immediate posttraumatic seizures and changes in corticosterone (CS) levels with neuroinflammation and neuronal cell loss in the hippocampus. Indices of distant hippocampal damage (neurodegeneration and neuroinflammation) were assessed using histological analysis (Nissl staining, Iba-1 immunohistochemical staining) and ELISA (IL-1β and CS) 1, 3, 7 and 14 days after TBI or sham operation in male Wistar rats (n = 146). IL-1β was elevated only in the ipsilateral hippocampus on day 1 after trauma. CS peak was detected on day 3 in blood, the ipsilateral and contralateral hippocampus. Neuronal cell loss in the hippocampus was demonstrated bilaterally; in the ipsilateral hippocampus it started earlier than in the contralateral. Microglial activation was evident in the hippocampus bilaterally on day 7 after TBI. The duration of immediate seizures correlated with CS elevation, levels of IL-1β and neuronal loss in the hippocampus. The data suggest potential association of immediate post-traumatic seizures with CS-dependent neuroinflammation-mediated distant hippocampal damage. |
| first_indexed | 2024-03-10T10:51:53Z |
| format | Article |
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| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T10:51:53Z |
| publishDate | 2021-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-9ffb404b800242819ba9fd04a3685dc22023-11-21T22:08:51ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-05-012211588310.3390/ijms22115883Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in RatsIlia G. Komoltsev0Stepan O. Frankevich1Natalia I. Shirobokova2Aleksandra A. Volkova3Mikhail V. Onufriev4Julia V. Moiseeva5Margarita R. Novikova6Natalia V. Gulyaeva7Laboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaLaboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 5A Butlerov Str., 117485 Moscow, RussiaHippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), we assessed potential association of immediate posttraumatic seizures and changes in corticosterone (CS) levels with neuroinflammation and neuronal cell loss in the hippocampus. Indices of distant hippocampal damage (neurodegeneration and neuroinflammation) were assessed using histological analysis (Nissl staining, Iba-1 immunohistochemical staining) and ELISA (IL-1β and CS) 1, 3, 7 and 14 days after TBI or sham operation in male Wistar rats (n = 146). IL-1β was elevated only in the ipsilateral hippocampus on day 1 after trauma. CS peak was detected on day 3 in blood, the ipsilateral and contralateral hippocampus. Neuronal cell loss in the hippocampus was demonstrated bilaterally; in the ipsilateral hippocampus it started earlier than in the contralateral. Microglial activation was evident in the hippocampus bilaterally on day 7 after TBI. The duration of immediate seizures correlated with CS elevation, levels of IL-1β and neuronal loss in the hippocampus. The data suggest potential association of immediate post-traumatic seizures with CS-dependent neuroinflammation-mediated distant hippocampal damage.https://www.mdpi.com/1422-0067/22/11/5883neuroinflammationneurodegenerationhippocampuscorticosteroneseizurestraumatic brain injury |
| spellingShingle | Ilia G. Komoltsev Stepan O. Frankevich Natalia I. Shirobokova Aleksandra A. Volkova Mikhail V. Onufriev Julia V. Moiseeva Margarita R. Novikova Natalia V. Gulyaeva Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats International Journal of Molecular Sciences neuroinflammation neurodegeneration hippocampus corticosterone seizures traumatic brain injury |
| title | Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats |
| title_full | Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats |
| title_fullStr | Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats |
| title_full_unstemmed | Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats |
| title_short | Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats |
| title_sort | neuroinflammation and neuronal loss in the hippocampus are associated with immediate posttraumatic seizures and corticosterone elevation in rats |
| topic | neuroinflammation neurodegeneration hippocampus corticosterone seizures traumatic brain injury |
| url | https://www.mdpi.com/1422-0067/22/11/5883 |
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