Early Electrophysiological Sequelae of Dosed Craniocerebral Trauma in Rats
Objectives. To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus. Materials and methods. Studies were performed using Sprague–Dawley rats. CCT was modeled using la...
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| Veröffentlicht in: | Neuroscience and behavioral physiology 2019-10, Vol.49 (8), p.1071-1075 |
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| creator | Komoltsev, I. G. Frankevich, S. O. Shirobokova, N. I. Volkova, A. A. Levshina, I. P. Novikova, M. R. Manolova, A. O. Gulyaeva, N. V. |
| description | Objectives.
To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus.
Materials and methods.
Studies were performed using Sprague–Dawley rats. CCT was modeled using lateral hydrodynamic blows to the sensorimotor cortex. Electrocorticograms were recorded one week before application of CCT and one week after CCT. Histological analysis was run one week after CCT. Sections were stained by the Nissl method and immunohistochemically for an astrocyte marker (GFAP) and microglia (isolectin B4). The extents of damage in the cortex and hippocampal were evaluated.
Results and conclusions.
Slowing of baseline activity was seen 1 and 6 h after CCT, and epileptiform activity appeared in 50% of the animals one week after CCT. The number of discharges correlated with the area of astrocyte gliosis in the cortex and the number of dark “ischemic” neurons in the hippocampus. Microglial activity in the hippocampus did not correlate with epileptiform activity. these data are important for understanding the early mechanisms of posttraumatic epileptogenesis. |
| doi_str_mv | 10.1007/s11055-019-00840-x |
| format | Article |
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To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus.
Materials and methods.
Studies were performed using Sprague–Dawley rats. CCT was modeled using lateral hydrodynamic blows to the sensorimotor cortex. Electrocorticograms were recorded one week before application of CCT and one week after CCT. Histological analysis was run one week after CCT. Sections were stained by the Nissl method and immunohistochemically for an astrocyte marker (GFAP) and microglia (isolectin B4). The extents of damage in the cortex and hippocampal were evaluated.
Results and conclusions.
Slowing of baseline activity was seen 1 and 6 h after CCT, and epileptiform activity appeared in 50% of the animals one week after CCT. The number of discharges correlated with the area of astrocyte gliosis in the cortex and the number of dark “ischemic” neurons in the hippocampus. Microglial activity in the hippocampus did not correlate with epileptiform activity. these data are important for understanding the early mechanisms of posttraumatic epileptogenesis.</description><identifier>ISSN: 0097-0549</identifier><identifier>EISSN: 1573-899X</identifier><identifier>DOI: 10.1007/s11055-019-00840-x</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Behavioral Sciences ; Biomedical and Life Sciences ; Biomedicine ; Complications ; Cortex (somatosensory) ; Epilepsy ; Glial fibrillary acidic protein ; Gliosis ; Hippocampus ; Ischemia ; Microglia ; Neurobiology ; Neurosciences ; Trauma</subject><ispartof>Neuroscience and behavioral physiology, 2019-10, Vol.49 (8), p.1071-1075</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Neuroscience and Behavioral Physiology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c234x-8286db19f169e867eff015605cc113590979a38bb3459988a2f2494b8df6f8113</citedby><cites>FETCH-LOGICAL-c234x-8286db19f169e867eff015605cc113590979a38bb3459988a2f2494b8df6f8113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11055-019-00840-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11055-019-00840-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids></links><search><creatorcontrib>Komoltsev, I. G.</creatorcontrib><creatorcontrib>Frankevich, S. O.</creatorcontrib><creatorcontrib>Shirobokova, N. I.</creatorcontrib><creatorcontrib>Volkova, A. A.</creatorcontrib><creatorcontrib>Levshina, I. P.</creatorcontrib><creatorcontrib>Novikova, M. R.</creatorcontrib><creatorcontrib>Manolova, A. O.</creatorcontrib><creatorcontrib>Gulyaeva, N. V.</creatorcontrib><title>Early Electrophysiological Sequelae of Dosed Craniocerebral Trauma in Rats</title><title>Neuroscience and behavioral physiology</title><addtitle>Neurosci Behav Physi</addtitle><description>Objectives.
To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus.
Materials and methods.
Studies were performed using Sprague–Dawley rats. CCT was modeled using lateral hydrodynamic blows to the sensorimotor cortex. Electrocorticograms were recorded one week before application of CCT and one week after CCT. Histological analysis was run one week after CCT. Sections were stained by the Nissl method and immunohistochemically for an astrocyte marker (GFAP) and microglia (isolectin B4). The extents of damage in the cortex and hippocampal were evaluated.
Results and conclusions.
Slowing of baseline activity was seen 1 and 6 h after CCT, and epileptiform activity appeared in 50% of the animals one week after CCT. The number of discharges correlated with the area of astrocyte gliosis in the cortex and the number of dark “ischemic” neurons in the hippocampus. Microglial activity in the hippocampus did not correlate with epileptiform activity. these data are important for understanding the early mechanisms of posttraumatic epileptogenesis.</description><subject>Behavioral Sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Complications</subject><subject>Cortex (somatosensory)</subject><subject>Epilepsy</subject><subject>Glial fibrillary acidic protein</subject><subject>Gliosis</subject><subject>Hippocampus</subject><subject>Ischemia</subject><subject>Microglia</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Trauma</subject><issn>0097-0549</issn><issn>1573-899X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kE1LAzEURYMoWKt_wFXAdfS9ySSTLKXWLwRBK7gLmWlSp0wnNWmh_fdGR3Dn6m3Ove9yCDlHuESA6iohghAMUDMAVQLbHZARioozpfX7IRkB6IqBKPUxOUlpCTlUKRiRx6mN3Z5OO9dsYlh_7FMburBoG9vRV_e5dZ11NHh6E5Kb00m0fRsaF10dMzCLdruytO3pi92kU3LkbZfc2e8dk7fb6Wxyz56e7x4m10-sKXi5Y6pQcl6j9ii1U7Jy3gMKCaJpELnQeai2XNU1L4XWStnCF6UuazX30quMjMnF0LuOIQ9MG7MM29jnl6bguR21RJmpYqCaGFKKzpt1bFc27g2C-XZmBmcmOzM_zswuh_gQShnuFy7-Vf-T-gLrKm6Z</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Komoltsev, I. G.</creator><creator>Frankevich, S. O.</creator><creator>Shirobokova, N. I.</creator><creator>Volkova, A. A.</creator><creator>Levshina, I. P.</creator><creator>Novikova, M. R.</creator><creator>Manolova, A. O.</creator><creator>Gulyaeva, N. 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I. ; Volkova, A. A. ; Levshina, I. P. ; Novikova, M. R. ; Manolova, A. O. ; Gulyaeva, N. V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c234x-8286db19f169e867eff015605cc113590979a38bb3459988a2f2494b8df6f8113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Behavioral Sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Complications</topic><topic>Cortex (somatosensory)</topic><topic>Epilepsy</topic><topic>Glial fibrillary acidic protein</topic><topic>Gliosis</topic><topic>Hippocampus</topic><topic>Ischemia</topic><topic>Microglia</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Trauma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Komoltsev, I. G.</creatorcontrib><creatorcontrib>Frankevich, S. O.</creatorcontrib><creatorcontrib>Shirobokova, N. I.</creatorcontrib><creatorcontrib>Volkova, A. A.</creatorcontrib><creatorcontrib>Levshina, I. P.</creatorcontrib><creatorcontrib>Novikova, M. R.</creatorcontrib><creatorcontrib>Manolova, A. O.</creatorcontrib><creatorcontrib>Gulyaeva, N. V.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Neuroscience and behavioral physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Komoltsev, I. G.</au><au>Frankevich, S. O.</au><au>Shirobokova, N. I.</au><au>Volkova, A. A.</au><au>Levshina, I. P.</au><au>Novikova, M. R.</au><au>Manolova, A. O.</au><au>Gulyaeva, N. V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Early Electrophysiological Sequelae of Dosed Craniocerebral Trauma in Rats</atitle><jtitle>Neuroscience and behavioral physiology</jtitle><stitle>Neurosci Behav Physi</stitle><date>2019-10-01</date><risdate>2019</risdate><volume>49</volume><issue>8</issue><spage>1071</spage><epage>1075</epage><pages>1071-1075</pages><issn>0097-0549</issn><eissn>1573-899X</eissn><abstract>Objectives.
To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus.
Materials and methods.
Studies were performed using Sprague–Dawley rats. CCT was modeled using lateral hydrodynamic blows to the sensorimotor cortex. Electrocorticograms were recorded one week before application of CCT and one week after CCT. Histological analysis was run one week after CCT. Sections were stained by the Nissl method and immunohistochemically for an astrocyte marker (GFAP) and microglia (isolectin B4). The extents of damage in the cortex and hippocampal were evaluated.
Results and conclusions.
Slowing of baseline activity was seen 1 and 6 h after CCT, and epileptiform activity appeared in 50% of the animals one week after CCT. The number of discharges correlated with the area of astrocyte gliosis in the cortex and the number of dark “ischemic” neurons in the hippocampus. Microglial activity in the hippocampus did not correlate with epileptiform activity. these data are important for understanding the early mechanisms of posttraumatic epileptogenesis.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s11055-019-00840-x</doi><tpages>5</tpages></addata></record> |
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| subjects | Behavioral Sciences Biomedical and Life Sciences Biomedicine Complications Cortex (somatosensory) Epilepsy Glial fibrillary acidic protein Gliosis Hippocampus Ischemia Microglia Neurobiology Neurosciences Trauma |
| title | Early Electrophysiological Sequelae of Dosed Craniocerebral Trauma in Rats |
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