Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury?
Alcohol-related traumatic brain injury (TBI) is a common condition in medical and forensic practice, and results in high prehospital mortality. We investigated the mechanism of chronic alcoholism-related mortality by examining the effects of alcohol on the synapses of the medulla oblongata in a rat...
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| Veröffentlicht in: | Cell biochemistry and biophysics 2013-12, Vol.67 (3), p.1049-1057 |
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| creator | Lai, Xiao-ping Yu, Xiao-jun Qian, Hong Wei, Lai Lv, Jun-yao Xu, Xiao-hu |
| description | Alcohol-related traumatic brain injury (TBI) is a common condition in medical and forensic practice, and results in high prehospital mortality. We investigated the mechanism of chronic alcoholism-related mortality by examining the effects of alcohol on the synapses of the medulla oblongata in a rat model of TBI. Seventy adult male Sprague–Dawley rats were randomly assigned to either ethanol (EtOH) group, EtOH-TBI group, or control groups (water group, water-TBI group). To establish chronic alcoholism model, rats in the EtOH group were given EtOH twice daily (4 g/kg for 2 weeks and 6 g/kg for another 2 weeks). The rats also received a minor strike on the occipital tuberosity with an iron pendulum. Histopathologic and ultrastructure changes and the numerical density of the synapses in the medulla oblongata were examined. Expression of postsynaptic density-95 (PSD-95) in the medulla oblongata was measured by ELISA. Compared with rats in the control group, rats in the chronic alcoholism group showed: (1) minor axonal degeneration; (2) a significant decrease in the numerical density of synapses (
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| doi_str_mv | 10.1007/s12013-013-9603-y |
| format | Article |
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p
< 0.01); and (3) compensatory increase in PSD-95 expression (
p
< 0.01). Rats in the EtOH-TBI group showed: (1) high mortality (50 %,
p
< 0.01); (2) inhibited respiration before death; (3) severe axonal injury; and (4) decrease in PSD-95 expression (
p
< 0.05). Chronic alcoholism induces significant synapse loss and axonal impairment in the medulla oblongata and renders the brain more susceptible to TBI. The combined effects of chronic alcoholism and TBI induce significant synapse and axon impairment and result in high mortality.</description><identifier>ISSN: 1085-9195</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-013-9603-y</identifier><identifier>PMID: 23546937</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Alcoholism ; Alcoholism - complications ; Animals ; Axons - drug effects ; Axons - metabolism ; Axons - ultrastructure ; Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Brain Injuries - complications ; Brain Injuries - metabolism ; Brain Injuries - mortality ; Cell Biology ; Disease Models, Animal ; Disks Large Homolog 4 Protein ; Ethanol ; Ethanol - toxicity ; Intracellular Signaling Peptides and Proteins - metabolism ; Life Sciences ; Male ; Medulla Oblongata - drug effects ; Medulla Oblongata - pathology ; Medulla Oblongata - ultrastructure ; Membrane Proteins - metabolism ; Mortality ; Original Paper ; Pharmacology/Toxicology ; Rats ; Rats, Sprague-Dawley ; Synapses - drug effects ; Synapses - metabolism ; Synapses - ultrastructure</subject><ispartof>Cell biochemistry and biophysics, 2013-12, Vol.67 (3), p.1049-1057</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-e61417dd9e9246d53de933601d9780476f7340e4e599f0a57e07700791e6bd093</citedby><cites>FETCH-LOGICAL-c372t-e61417dd9e9246d53de933601d9780476f7340e4e599f0a57e07700791e6bd093</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/s12013-013-9603-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-013-9603-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23546937$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Xiao-ping</creatorcontrib><creatorcontrib>Yu, Xiao-jun</creatorcontrib><creatorcontrib>Qian, Hong</creatorcontrib><creatorcontrib>Wei, Lai</creatorcontrib><creatorcontrib>Lv, Jun-yao</creatorcontrib><creatorcontrib>Xu, Xiao-hu</creatorcontrib><title>Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury?</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><addtitle>Cell Biochem Biophys</addtitle><description>Alcohol-related traumatic brain injury (TBI) is a common condition in medical and forensic practice, and results in high prehospital mortality. We investigated the mechanism of chronic alcoholism-related mortality by examining the effects of alcohol on the synapses of the medulla oblongata in a rat model of TBI. Seventy adult male Sprague–Dawley rats were randomly assigned to either ethanol (EtOH) group, EtOH-TBI group, or control groups (water group, water-TBI group). To establish chronic alcoholism model, rats in the EtOH group were given EtOH twice daily (4 g/kg for 2 weeks and 6 g/kg for another 2 weeks). The rats also received a minor strike on the occipital tuberosity with an iron pendulum. Histopathologic and ultrastructure changes and the numerical density of the synapses in the medulla oblongata were examined. Expression of postsynaptic density-95 (PSD-95) in the medulla oblongata was measured by ELISA. Compared with rats in the control group, rats in the chronic alcoholism group showed: (1) minor axonal degeneration; (2) a significant decrease in the numerical density of synapses (
p
< 0.01); and (3) compensatory increase in PSD-95 expression (
p
< 0.01). Rats in the EtOH-TBI group showed: (1) high mortality (50 %,
p
< 0.01); (2) inhibited respiration before death; (3) severe axonal injury; and (4) decrease in PSD-95 expression (
p
< 0.05). Chronic alcoholism induces significant synapse loss and axonal impairment in the medulla oblongata and renders the brain more susceptible to TBI. The combined effects of chronic alcoholism and TBI induce significant synapse and axon impairment and result in high mortality.</description><subject>Alcoholism</subject><subject>Alcoholism - complications</subject><subject>Animals</subject><subject>Axons - drug effects</subject><subject>Axons - metabolism</subject><subject>Axons - ultrastructure</subject><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Brain Injuries - complications</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - mortality</subject><subject>Cell Biology</subject><subject>Disease Models, Animal</subject><subject>Disks Large Homolog 4 Protein</subject><subject>Ethanol</subject><subject>Ethanol - toxicity</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medulla Oblongata - drug effects</subject><subject>Medulla Oblongata - pathology</subject><subject>Medulla Oblongata - ultrastructure</subject><subject>Membrane Proteins - metabolism</subject><subject>Mortality</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Synapses - drug effects</subject><subject>Synapses - metabolism</subject><subject>Synapses - ultrastructure</subject><issn>1085-9195</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1v1DAQhi1ERT_gB3BBkbhwMR3HdhxzQcuqwEqtKqFyjrzxpJtVYi-2c8idH47DtghV6mFkj-eZd2y_hLxl8JEBqMvISmCcLqEr4HR-Qc6YlJpCWfOXeQ-1pJppeUrOY9wDlCUI8YqcllyKSnN1Rn6vd8G7vi1WQ-t3fujjSG_Q9iahLTbjwfRhRJeK3hVph0UuTcNgitvt4N29SeZTscqH7c643Fn47lGH_sDhr8aND8kMfZoXibtgptGkPO5LMDnfuP0U5s-vyUlnhohvHtYL8vPr1d36O72-_bZZr65py1WZKFZMMGWtRl2KykpuUXNeAbNa1SBU1SkuAAVKrTswUiEolf9JM6y2FjS_IB-Ouofgf00YUzP2scX8IId-ig0TFasVU7XM6Psn6N5PweXbLRTUvGaizhQ7Um3wMQbsmkPoRxPmhkGzWNQcLWqWWCxq5tzz7kF52o5o_3U8epKB8gjEXHL3GP4b_azqH7oem2g</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Lai, Xiao-ping</creator><creator>Yu, Xiao-jun</creator><creator>Qian, Hong</creator><creator>Wei, Lai</creator><creator>Lv, Jun-yao</creator><creator>Xu, Xiao-hu</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20131201</creationdate><title>Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury?</title><author>Lai, Xiao-ping ; Yu, Xiao-jun ; Qian, Hong ; Wei, Lai ; Lv, Jun-yao ; Xu, Xiao-hu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-e61417dd9e9246d53de933601d9780476f7340e4e599f0a57e07700791e6bd093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alcoholism</topic><topic>Alcoholism - 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drug effects</topic><topic>Synapses - metabolism</topic><topic>Synapses - ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lai, Xiao-ping</creatorcontrib><creatorcontrib>Yu, Xiao-jun</creatorcontrib><creatorcontrib>Qian, Hong</creatorcontrib><creatorcontrib>Wei, Lai</creatorcontrib><creatorcontrib>Lv, Jun-yao</creatorcontrib><creatorcontrib>Xu, Xiao-hu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Xiao-ping</au><au>Yu, Xiao-jun</au><au>Qian, Hong</au><au>Wei, Lai</au><au>Lv, Jun-yao</au><au>Xu, Xiao-hu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury?</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><addtitle>Cell Biochem Biophys</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>67</volume><issue>3</issue><spage>1049</spage><epage>1057</epage><pages>1049-1057</pages><issn>1085-9195</issn><eissn>1559-0283</eissn><abstract>Alcohol-related traumatic brain injury (TBI) is a common condition in medical and forensic practice, and results in high prehospital mortality. We investigated the mechanism of chronic alcoholism-related mortality by examining the effects of alcohol on the synapses of the medulla oblongata in a rat model of TBI. Seventy adult male Sprague–Dawley rats were randomly assigned to either ethanol (EtOH) group, EtOH-TBI group, or control groups (water group, water-TBI group). To establish chronic alcoholism model, rats in the EtOH group were given EtOH twice daily (4 g/kg for 2 weeks and 6 g/kg for another 2 weeks). The rats also received a minor strike on the occipital tuberosity with an iron pendulum. Histopathologic and ultrastructure changes and the numerical density of the synapses in the medulla oblongata were examined. Expression of postsynaptic density-95 (PSD-95) in the medulla oblongata was measured by ELISA. Compared with rats in the control group, rats in the chronic alcoholism group showed: (1) minor axonal degeneration; (2) a significant decrease in the numerical density of synapses (
p
< 0.01); and (3) compensatory increase in PSD-95 expression (
p
< 0.01). Rats in the EtOH-TBI group showed: (1) high mortality (50 %,
p
< 0.01); (2) inhibited respiration before death; (3) severe axonal injury; and (4) decrease in PSD-95 expression (
p
< 0.05). Chronic alcoholism induces significant synapse loss and axonal impairment in the medulla oblongata and renders the brain more susceptible to TBI. The combined effects of chronic alcoholism and TBI induce significant synapse and axon impairment and result in high mortality.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23546937</pmid><doi>10.1007/s12013-013-9603-y</doi><tpages>9</tpages></addata></record> |
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| subjects | Alcoholism Alcoholism - complications Animals Axons - drug effects Axons - metabolism Axons - ultrastructure Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Brain Injuries - complications Brain Injuries - metabolism Brain Injuries - mortality Cell Biology Disease Models, Animal Disks Large Homolog 4 Protein Ethanol Ethanol - toxicity Intracellular Signaling Peptides and Proteins - metabolism Life Sciences Male Medulla Oblongata - drug effects Medulla Oblongata - pathology Medulla Oblongata - ultrastructure Membrane Proteins - metabolism Mortality Original Paper Pharmacology/Toxicology Rats Rats, Sprague-Dawley Synapses - drug effects Synapses - metabolism Synapses - ultrastructure |
| title | Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury? |
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