Loading…

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...

Full description

Saved in:
Bibliographic Details
Published in:Journal of environmental biology 2019-09, Vol.40 (5(SI)), p.833-840
Main Authors: Yu, Y.H., Kang, J.H., Lee, K.H., Yoo, D.Y., Park, D.K., Kim, D.S.
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 840
container_issue 5(SI)
container_start_page 833
container_title Journal of environmental biology
container_volume 40
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
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2296125549</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2296125549</sourcerecordid><originalsourceid>FETCH-LOGICAL-c271t-b28de10a74076fb1860cf8e194004d9f91ef49146a26ec92df2f183752b3a1c03</originalsourceid><addsrcrecordid>eNotkFtLxDAQhYMouKz7C3wp-KIPtZNLL3lcFi-FBR9Wn0OaJm5K29SkRfbfG10HDsMw35yBg9AthkdCGK2yTjcZgyy_P9QP2aFOgVygFaGcpUBLfolWQHKWViWwa7QJoYNYlJMy5yukt_2svW4TOwzL6I42zE4d9WCV7JM2Tt42y2zdmDiTHO00OSWHKe7sGO9GvXg3hsS4vnffdvxMZi-XQc5WJY2XdoxYt_jTDboysg9689_X6OP56X33mu7fXurddp8qUuI5bUjVagyyZFAWpsFVAcpUGnMGwFpuONaGccwKSQqtOGkNMbiiZU4aKrECukZ3Z9_Ju69Fh1l0bvFjfCkI4QUmec54pOiZUt6F4LURk7eD9CeBQfxFKmKkgoHIxaEWvwJCfwD8vm2P</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2296125549</pqid></control><display><type>article</type><title>Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury</title><source>EZB Electronic Journals Library</source><creator>Yu, Y.H. ; Kang, J.H. ; Lee, K.H. ; Yoo, D.Y. ; Park, D.K. ; Kim, D.S.</creator><creatorcontrib>Yu, Y.H. ; Kang, J.H. ; Lee, K.H. ; Yoo, D.Y. ; Park, D.K. ; Kim, D.S. ; Department of Anatomy, Soonchunhyang University, Cheonan, 31151, Republic of Korea</creatorcontrib><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><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 &amp; 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 &amp; 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 brain injury</subject><subject>Variance analysis</subject><issn>0254-8704</issn><issn>2394-0379</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNotkFtLxDAQhYMouKz7C3wp-KIPtZNLL3lcFi-FBR9Wn0OaJm5K29SkRfbfG10HDsMw35yBg9AthkdCGK2yTjcZgyy_P9QP2aFOgVygFaGcpUBLfolWQHKWViWwa7QJoYNYlJMy5yukt_2svW4TOwzL6I42zE4d9WCV7JM2Tt42y2zdmDiTHO00OSWHKe7sGO9GvXg3hsS4vnffdvxMZi-XQc5WJY2XdoxYt_jTDboysg9689_X6OP56X33mu7fXurddp8qUuI5bUjVagyyZFAWpsFVAcpUGnMGwFpuONaGccwKSQqtOGkNMbiiZU4aKrECukZ3Z9_Ju69Fh1l0bvFjfCkI4QUmec54pOiZUt6F4LURk7eD9CeBQfxFKmKkgoHIxaEWvwJCfwD8vm2P</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Yu, Y.H.</creator><creator>Kang, J.H.</creator><creator>Lee, K.H.</creator><creator>Yoo, D.Y.</creator><creator>Park, D.K.</creator><creator>Kim, D.S.</creator><general>Triveni 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 &amp; 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 &amp; Technology</collection><collection>ProQuest Central (Corporate)</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>ProQuest Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 &amp; Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Agriculture &amp; Environmental Science Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Engineering Collection</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest Engineering Database</collection><collection>Environmental Science Database</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Environment Abstracts</collection><jtitle>Journal of environmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Y.H.</au><au>Kang, J.H.</au><au>Lee, K.H.</au><au>Yoo, D.Y.</au><au>Park, D.K.</au><au>Kim, D.S.</au><aucorp>Department of Anatomy, Soonchunhyang University, Cheonan, 31151, Republic of Korea</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered immunohistochemical distribution of hippocampal interneurons following traumatic brain injury</atitle><jtitle>Journal of environmental 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>
fulltext fulltext
identifier ISSN: 0254-8704
ispartof Journal of environmental biology, 2019-09, Vol.40 (5(SI)), p.833-840
issn 0254-8704
2394-0379
language eng
recordid cdi_proquest_journals_2296125549
source EZB Electronic Journals Library
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
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-23T05%3A19%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Altered%20immunohistochemical%20distribution%20of%20hippocampal%20interneurons%20following%20traumatic%20brain%20injury&rft.jtitle=Journal%20of%20environmental%20biology&rft.au=Yu,%20Y.H.&rft.aucorp=Department%20of%20Anatomy,%20Soonchunhyang%20University,%20Cheonan,%2031151,%20Republic%20of%20Korea&rft.date=2019-09-01&rft.volume=40&rft.issue=5(SI)&rft.spage=833&rft.epage=840&rft.pages=833-840&rft.issn=0254-8704&rft.eissn=2394-0379&rft_id=info:doi/10.22438/jeb/40/5(SI)/SI-02&rft_dat=%3Cproquest_cross%3E2296125549%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c271t-b28de10a74076fb1860cf8e194004d9f91ef49146a26ec92df2f183752b3a1c03%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2296125549&rft_id=info:pmid/&rfr_iscdi=true