Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study
In order to determine the extent and duration of calcium (Ca 2+) flux following a lateral fluid percussion brain injury in the rat, 45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent...
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Veröffentlicht in: | Brain research 1993-10, Vol.624 (1), p.94-102 |
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creator | Fineman, Igor Hovda, David A. Smith, Mayumi Yoshino, Atsuo Becker, Donald P. |
description | In order to determine the extent and duration of calcium (Ca
2+) flux following a lateral fluid percussion brain injury in the rat,
45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of
45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of
45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage,
45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of
45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca
2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca
2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca
2+ can continue for at least 48 h. |
doi_str_mv | 10.1016/0006-8993(93)90064-T |
format | Article |
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2+) flux following a lateral fluid percussion brain injury in the rat,
45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of
45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of
45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage,
45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of
45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca
2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca
2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca
2+ can continue for at least 48 h.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0006-8993(93)90064-T</identifier><identifier>PMID: 8252419</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>45Calcium ; Animals ; Autoradiography ; Biological and medical sciences ; Brain - metabolism ; Brain - pathology ; Brain Concussion - metabolism ; Brain Concussion - pathology ; Calcium ; Calcium - metabolism ; Calcium Radioisotopes ; Cerebral concussion ; Contusion ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Rats ; Rats, Sprague-Dawley ; Traumas. Diseases due to physical agents ; Traumatic brain injury</subject><ispartof>Brain research, 1993-10, Vol.624 (1), p.94-102</ispartof><rights>1993 Elsevier Science Publishers B.V. All rights reserved</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1889-2fcb4838383d278272664777275c2cd1b14d0f191f7cc56671233e95022347853</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0006-8993(93)90064-T$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4886712$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8252419$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fineman, Igor</creatorcontrib><creatorcontrib>Hovda, David A.</creatorcontrib><creatorcontrib>Smith, Mayumi</creatorcontrib><creatorcontrib>Yoshino, Atsuo</creatorcontrib><creatorcontrib>Becker, Donald P.</creatorcontrib><title>Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>In order to determine the extent and duration of calcium (Ca
2+) flux following a lateral fluid percussion brain injury in the rat,
45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of
45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of
45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage,
45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of
45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca
2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca
2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca
2+ can continue for at least 48 h.</description><subject>45Calcium</subject><subject>Animals</subject><subject>Autoradiography</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Concussion - metabolism</subject><subject>Brain Concussion - pathology</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium Radioisotopes</subject><subject>Cerebral concussion</subject><subject>Contusion</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Traumatic brain injury</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kduKFDEQhoMo6-zoGyjkQkQvWnPqHPZCkGE9wII343XIVNK7Wbo7Y9JZmbc37Q5LCsKf-qhK1Y_QG0o-UULlZ0KI7LQx_IPhH00Tots_QxuqFeskE-Q52jwhL9FlKfdNcm7IBbrQrGeCmg2admmGWkp8CPiQXZxxnO9rPuFYsCslQXRL8PhvXO6ww8ecxjTftgcHUKc6uiWmGacBgxsh1umqQaLfOezqkrLzMd1md7yLgMtS_ekVejG4sYTX53uLfn-73u9-dDe_vv_cfb3pgGptOjbAQWi-Hs-UZopJKZRSTPXAwNMDFZ4M1NBBAfRSKso4D6YnjHGhdM-36P1j3fbhPzWUxU6xQBhHN4dUi1WSUmqEbODbM1gPU_D2mOPk8sme99Py7855V9qIQ3YzxPKECa3_N9-iL49YaEM9xJBtgRhmCD7mAIv1KVpK7GqbXT2xqyd2jdU2u-f_AMoFh9o</recordid><startdate>19931008</startdate><enddate>19931008</enddate><creator>Fineman, Igor</creator><creator>Hovda, David A.</creator><creator>Smith, Mayumi</creator><creator>Yoshino, Atsuo</creator><creator>Becker, Donald P.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19931008</creationdate><title>Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study</title><author>Fineman, Igor ; Hovda, David A. ; Smith, Mayumi ; Yoshino, Atsuo ; Becker, Donald P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1889-2fcb4838383d278272664777275c2cd1b14d0f191f7cc56671233e95022347853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>45Calcium</topic><topic>Animals</topic><topic>Autoradiography</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Concussion - metabolism</topic><topic>Brain Concussion - pathology</topic><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>Calcium Radioisotopes</topic><topic>Cerebral concussion</topic><topic>Contusion</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fineman, Igor</creatorcontrib><creatorcontrib>Hovda, David A.</creatorcontrib><creatorcontrib>Smith, Mayumi</creatorcontrib><creatorcontrib>Yoshino, Atsuo</creatorcontrib><creatorcontrib>Becker, Donald P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fineman, Igor</au><au>Hovda, David A.</au><au>Smith, Mayumi</au><au>Yoshino, Atsuo</au><au>Becker, Donald P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1993-10-08</date><risdate>1993</risdate><volume>624</volume><issue>1</issue><spage>94</spage><epage>102</epage><pages>94-102</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>In order to determine the extent and duration of calcium (Ca
2+) flux following a lateral fluid percussion brain injury in the rat,
45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of
45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of
45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage,
45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of
45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca
2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca
2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca
2+ can continue for at least 48 h.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>8252419</pmid><doi>10.1016/0006-8993(93)90064-T</doi><tpages>9</tpages></addata></record> |
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source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
subjects | 45Calcium Animals Autoradiography Biological and medical sciences Brain - metabolism Brain - pathology Brain Concussion - metabolism Brain Concussion - pathology Calcium Calcium - metabolism Calcium Radioisotopes Cerebral concussion Contusion Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences Rats Rats, Sprague-Dawley Traumas. Diseases due to physical agents Traumatic brain injury |
title | Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study |
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