Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding
Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The pr...
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| Veröffentlicht in: | Journal of neurotrauma 1999-10, Vol.16 (10), p.865-877 |
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| creator | RAGHAVENDRA RAO, V. L DOGAN, A BOWEN, K. K DEMPSEY, R. J |
| description | Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L-[3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI. |
| doi_str_mv | 10.1089/neu.1999.16.865 |
| format | Article |
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L ; DOGAN, A ; BOWEN, K. K ; DEMPSEY, R. J</creator><creatorcontrib>RAGHAVENDRA RAO, V. L ; DOGAN, A ; BOWEN, K. K ; DEMPSEY, R. J</creatorcontrib><description>Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L-[3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.1999.16.865</identifier><identifier>PMID: 10547096</identifier><identifier>CODEN: JNEUE4</identifier><language>eng</language><publisher>Larchmont, NY: Liebert</publisher><subject>Animals ; Biological and medical sciences ; Brain Injuries - enzymology ; Brain Injuries - physiopathology ; Functional Laterality ; Gene Expression Regulation, Enzymologic ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type I ; Nitroarginine - pharmacokinetics ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Transcription, Genetic ; Traumas. 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L</creatorcontrib><creatorcontrib>DOGAN, A</creatorcontrib><creatorcontrib>BOWEN, K. K</creatorcontrib><creatorcontrib>DEMPSEY, R. J</creatorcontrib><title>Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L-[3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain Injuries - enzymology</subject><subject>Brain Injuries - physiopathology</subject><subject>Functional Laterality</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type I</subject><subject>Nitroarginine - pharmacokinetics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Transcription, Genetic</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Tritium</subject><issn>0897-7151</issn><issn>1557-9042</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpN0UFLwzAUB_AgipvTszfJQby1S9IlbY4i6oSBl3kSCWmSzow2nUkK27c3ZQM9vcvvvcf7PwBuMcoxqvjcmSHHnPMcs7xi9AxMMaVlxtGCnINpEmVWYoon4CqELUK4YKS8BBOM6KJEnE1BWHs5dDJaBa3bDv4AYw-9jLD20jo47LzZDK2MJsC0y_dOttDZ6JPv91YbGA4ufstgoNknG4LtHZROw1X2WSy_RtpLv7HOOgNr67R1m2tw0cg2mJtTnYGPl-f10zJbvb--PT2uMlUQEjNS12RRalIwTRtEKk6QVppgXXFVN6bCplDEUKQI5ZoTwlCjSkSULrTijLJiBh6Oc3e-_xlMiKKzQZm2lc70QxAsNVFOeILzI1S-D8GbRuy87aQ_CIzEmLNIt4sxZ4GZSDmnjrvT6KHujP7nj8EmcH8CMijZNl46ZcOf4-X4jOIXXx-IkA</recordid><startdate>19991001</startdate><enddate>19991001</enddate><creator>RAGHAVENDRA RAO, V. L</creator><creator>DOGAN, A</creator><creator>BOWEN, K. K</creator><creator>DEMPSEY, R. J</creator><general>Liebert</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19991001</creationdate><title>Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding</title><author>RAGHAVENDRA RAO, V. L ; DOGAN, A ; BOWEN, K. K ; DEMPSEY, R. J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c322t-2bb247d236d5f028920dcd21d89cbfe81e3c2e50c259d92260fc702cd3dc96563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain Injuries - enzymology</topic><topic>Brain Injuries - physiopathology</topic><topic>Functional Laterality</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type I</topic><topic>Nitroarginine - pharmacokinetics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Transcription, Genetic</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Tritium</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RAGHAVENDRA RAO, V. L</creatorcontrib><creatorcontrib>DOGAN, A</creatorcontrib><creatorcontrib>BOWEN, K. K</creatorcontrib><creatorcontrib>DEMPSEY, R. 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J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding</atitle><jtitle>Journal of neurotrauma</jtitle><addtitle>J Neurotrauma</addtitle><date>1999-10-01</date><risdate>1999</risdate><volume>16</volume><issue>10</issue><spage>865</spage><epage>877</epage><pages>865-877</pages><issn>0897-7151</issn><eissn>1557-9042</eissn><coden>JNEUE4</coden><abstract>Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L-[3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI.</abstract><cop>Larchmont, NY</cop><pub>Liebert</pub><pmid>10547096</pmid><doi>10.1089/neu.1999.16.865</doi><tpages>13</tpages></addata></record> |
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| source | Mary Ann Liebert Online Subscription; MEDLINE |
| subjects | Animals Biological and medical sciences Brain Injuries - enzymology Brain Injuries - physiopathology Functional Laterality Gene Expression Regulation, Enzymologic Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type I Nitroarginine - pharmacokinetics Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Transcription, Genetic Traumas. Diseases due to physical agents Tritium |
| title | Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding |
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