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Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury
Aim: The aim of this study was to determine whether alteration of interneurons in the hippocampus might play a role in neuronal damage caused by brain trauma and whether immunohisto chemical expressions in the hippocampus might change during the adaptive stage as early time point following traumatic...
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Published in: | Journal of environmental biology 2019-09, Vol.40 (5(SI)), p.833-840 |
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creator | Yu, Y.H. Kang, J.H. Lee, K.H. Yoo, D.Y. Park, D.K. Kim, D.S. |
description | Aim: The aim of this study was to determine whether alteration of interneurons in the hippocampus might play a role in neuronal damage caused by brain trauma and whether immunohisto chemical expressions in the hippocampus might change during the adaptive stage as early time point following traumatic brain injury (TBI). Methodology: For the study, we used Sprague-Dawley (SD) rats and manufactured TBI animal model by creating cryogenic injury to specific brain tissue. Thereafter, immunohisto chemical approaches were utilized to determine parvalbumin (PV) and calbindin D-28K (CB) expression in the hippocampus following brain trauma in a time course. All hippocampal tissues were analyzed qualitatively and quantitatively using immunoreactivity, cell counting and densitometry. Statistical significance was determined by one-way ANOVA and Bonferroni's test. Results: At early time period following TBI, both PVand CB immunoreactivities decreased in the lesioned hippocampus. However, their expression levels were recovered to control levels as time passed by. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced whereas CB expression remained unchanged. Interpretation: Results of this study revealed that altered distribution of interneuronal populations in the hippocampus might contribute to neuronal loss induced by abnormality of inhibitory neurotransmission at early time period following brain damage, thus leading to the development of epileptogenesis in patients with TBI. |
doi_str_mv | 10.22438/jeb/40/5(SI)/SI-02 |
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Methodology: For the study, we used Sprague-Dawley (SD) rats and manufactured TBI animal model by creating cryogenic injury to specific brain tissue. Thereafter, immunohisto chemical approaches were utilized to determine parvalbumin (PV) and calbindin D-28K (CB) expression in the hippocampus following brain trauma in a time course. All hippocampal tissues were analyzed qualitatively and quantitatively using immunoreactivity, cell counting and densitometry. Statistical significance was determined by one-way ANOVA and Bonferroni's test. Results: At early time period following TBI, both PVand CB immunoreactivities decreased in the lesioned hippocampus. However, their expression levels were recovered to control levels as time passed by. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced whereas CB expression remained unchanged. Interpretation: Results of this study revealed that altered distribution of interneuronal populations in the hippocampus might contribute to neuronal loss induced by abnormality of inhibitory neurotransmission at early time period following brain damage, thus leading to the development of epileptogenesis in patients with TBI.</description><identifier>ISSN: 0254-8704</identifier><identifier>EISSN: 2394-0379</identifier><identifier>DOI: 10.22438/jeb/40/5(SI)/SI-02</identifier><language>eng</language><publisher>Lucknow: Triveni Enterprises</publisher><subject>Animal models ; Brain ; Brain damage ; Calbindin-D28K ; Convulsions & seizures ; Densitometers ; Densitometry ; Epilepsy ; Head injuries ; Hippocampus ; Immunoreactivity ; Interneurons ; Laboratory animals ; Medical prognosis ; Neurotransmission ; Organic chemistry ; Parvalbumin ; Pathogenesis ; Rodents ; Trauma ; Traumatic brain injury ; Variance analysis</subject><ispartof>Journal of environmental biology, 2019-09, Vol.40 (5(SI)), p.833-840</ispartof><rights>Copyright Triveni Enterprises Sep 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids></links><search><creatorcontrib>Yu, Y.H.</creatorcontrib><creatorcontrib>Kang, J.H.</creatorcontrib><creatorcontrib>Lee, K.H.</creatorcontrib><creatorcontrib>Yoo, D.Y.</creatorcontrib><creatorcontrib>Park, D.K.</creatorcontrib><creatorcontrib>Kim, D.S.</creatorcontrib><creatorcontrib>Department of Anatomy, Soonchunhyang University, Cheonan, 31151, Republic of Korea</creatorcontrib><title>Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury</title><title>Journal of environmental biology</title><description>Aim: The aim of this study was to determine whether alteration of interneurons in the hippocampus might play a role in neuronal damage caused by brain trauma and whether immunohisto chemical expressions in the hippocampus might change during the adaptive stage as early time point following traumatic brain injury (TBI). Methodology: For the study, we used Sprague-Dawley (SD) rats and manufactured TBI animal model by creating cryogenic injury to specific brain tissue. Thereafter, immunohisto chemical approaches were utilized to determine parvalbumin (PV) and calbindin D-28K (CB) expression in the hippocampus following brain trauma in a time course. All hippocampal tissues were analyzed qualitatively and quantitatively using immunoreactivity, cell counting and densitometry. Statistical significance was determined by one-way ANOVA and Bonferroni's test. Results: At early time period following TBI, both PVand CB immunoreactivities decreased in the lesioned hippocampus. However, their expression levels were recovered to control levels as time passed by. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced whereas CB expression remained unchanged. Interpretation: Results of this study revealed that altered distribution of interneuronal populations in the hippocampus might contribute to neuronal loss induced by abnormality of inhibitory neurotransmission at early time period following brain damage, thus leading to the development of epileptogenesis in patients with TBI.</description><subject>Animal models</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Calbindin-D28K</subject><subject>Convulsions & seizures</subject><subject>Densitometers</subject><subject>Densitometry</subject><subject>Epilepsy</subject><subject>Head injuries</subject><subject>Hippocampus</subject><subject>Immunoreactivity</subject><subject>Interneurons</subject><subject>Laboratory animals</subject><subject>Medical prognosis</subject><subject>Neurotransmission</subject><subject>Organic chemistry</subject><subject>Parvalbumin</subject><subject>Pathogenesis</subject><subject>Rodents</subject><subject>Trauma</subject><subject>Traumatic 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Enterprises</general><scope>AAYXX</scope><scope>CITATION</scope><scope>04Q</scope><scope>04W</scope><scope>3V.</scope><scope>7ST</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>SOI</scope></search><sort><creationdate>20190901</creationdate><title>Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury</title><author>Yu, Y.H. ; Kang, J.H. ; Lee, K.H. ; Yoo, D.Y. ; Park, D.K. ; Kim, D.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c271t-b28de10a74076fb1860cf8e194004d9f91ef49146a26ec92df2f183752b3a1c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animal models</topic><topic>Brain</topic><topic>Brain damage</topic><topic>Calbindin-D28K</topic><topic>Convulsions & seizures</topic><topic>Densitometers</topic><topic>Densitometry</topic><topic>Epilepsy</topic><topic>Head injuries</topic><topic>Hippocampus</topic><topic>Immunoreactivity</topic><topic>Interneurons</topic><topic>Laboratory animals</topic><topic>Medical prognosis</topic><topic>Neurotransmission</topic><topic>Organic chemistry</topic><topic>Parvalbumin</topic><topic>Pathogenesis</topic><topic>Rodents</topic><topic>Trauma</topic><topic>Traumatic brain injury</topic><topic>Variance analysis</topic><toplevel>online_resources</toplevel><creatorcontrib>Yu, Y.H.</creatorcontrib><creatorcontrib>Kang, J.H.</creatorcontrib><creatorcontrib>Lee, K.H.</creatorcontrib><creatorcontrib>Yoo, D.Y.</creatorcontrib><creatorcontrib>Park, D.K.</creatorcontrib><creatorcontrib>Kim, D.S.</creatorcontrib><creatorcontrib>Department of Anatomy, Soonchunhyang University, Cheonan, 31151, Republic of Korea</creatorcontrib><collection>CrossRef</collection><collection>India Database</collection><collection>India Database: Science & Technology</collection><collection>ProQuest Central (Corporate)</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 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biology</jtitle><date>2019-09-01</date><risdate>2019</risdate><volume>40</volume><issue>5(SI)</issue><spage>833</spage><epage>840</epage><pages>833-840</pages><issn>0254-8704</issn><eissn>2394-0379</eissn><abstract>Aim: The aim of this study was to determine whether alteration of interneurons in the hippocampus might play a role in neuronal damage caused by brain trauma and whether immunohisto chemical expressions in the hippocampus might change during the adaptive stage as early time point following traumatic brain injury (TBI). Methodology: For the study, we used Sprague-Dawley (SD) rats and manufactured TBI animal model by creating cryogenic injury to specific brain tissue. Thereafter, immunohisto chemical approaches were utilized to determine parvalbumin (PV) and calbindin D-28K (CB) expression in the hippocampus following brain trauma in a time course. All hippocampal tissues were analyzed qualitatively and quantitatively using immunoreactivity, cell counting and densitometry. Statistical significance was determined by one-way ANOVA and Bonferroni's test. Results: At early time period following TBI, both PVand CB immunoreactivities decreased in the lesioned hippocampus. However, their expression levels were recovered to control levels as time passed by. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced whereas CB expression remained unchanged. Interpretation: Results of this study revealed that altered distribution of interneuronal populations in the hippocampus might contribute to neuronal loss induced by abnormality of inhibitory neurotransmission at early time period following brain damage, thus leading to the development of epileptogenesis in patients with TBI.</abstract><cop>Lucknow</cop><pub>Triveni Enterprises</pub><doi>10.22438/jeb/40/5(SI)/SI-02</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animal models Brain Brain damage Calbindin-D28K Convulsions & seizures Densitometers Densitometry Epilepsy Head injuries Hippocampus Immunoreactivity Interneurons Laboratory animals Medical prognosis Neurotransmission Organic chemistry Parvalbumin Pathogenesis Rodents Trauma Traumatic brain injury Variance analysis |
title | Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury |
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