Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury
Abstract Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague–Dawley rats ( n =5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted...
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| creator | Kabatas, S Yu, D He, X.D Thatte, H.S Benedict, D Hepgul, K.T Black, P.M Sabharwal, S Teng, Y.D |
| description | Abstract Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague–Dawley rats ( n =5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted for 24 h before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (−64.1% and −49.5%) and ileum (−73.6% and −70.1%) at 48 h and 4 weeks p.i., respectively ( P ≤0.005, ANOVA with post hoc t -test). Electrophysiological analysis revealed that purinergic fast inhibitory junction potential (IJP) was reduced ∼30% in the antrum and duodenum of rats 48 h p.i. (numbers of animals/numbers of tissue samples=3/7; P |
| doi_str_mv | 10.1016/j.neuroscience.2008.04.071 |
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In this study, female Sprague–Dawley rats ( n =5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted for 24 h before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (−64.1% and −49.5%) and ileum (−73.6% and −70.1%) at 48 h and 4 weeks p.i., respectively ( P ≤0.005, ANOVA with post hoc t -test). Electrophysiological analysis revealed that purinergic fast inhibitory junction potential (IJP) was reduced ∼30% in the antrum and duodenum of rats 48 h p.i. (numbers of animals/numbers of tissue samples=3/7; P <0.001), and slow IJP was essentially abolished. Immunocytochemistry consequently uncovered significant reductions in the GI vasoactive intestinal polypeptide and neuronal nitric oxide synthase (i.e. slow IJP mediators) reactivity at 48 h and 4 weeks p.i., suggesting that SCI disrupted interstitial neurotransmission. Importantly, SCI caused discernible atrophy of the GI mucosa and muscle coat (e.g. the two layers of gastric wall were correspondingly 28% and 27% thinner 4 weeks p.i.). We conclude that contusive SCI triggers GI abnormalities with unique pathophysiology and pathology in different segments. Such GI disorders evolve continuously during the entire post-SCI period examined, and may require therapeutic development to target specific underlying mechanisms.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2008.04.071</identifier><identifier>PMID: 18556138</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Female ; Fundamental and applied biological sciences. Psychology ; Gastrointestinal Diseases - etiology ; Gastrointestinal Diseases - pathology ; Gastrointestinal Diseases - physiopathology ; gastrointestinal dysfunction ; Gastrointestinal Tract - innervation ; Gastrointestinal Tract - pathology ; Gastrointestinal Tract - physiopathology ; Gastrointestinal Transit - physiology ; IJP ; Immunohistochemistry ; Membrane Potentials - physiology ; Neurology ; Nitric Oxide Synthase Type I - biosynthesis ; nNOS ; rat ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries - complications ; Spinal Cord Injuries - physiopathology ; spinal cord injury ; Vasoactive Intestinal Peptide - biosynthesis ; Vertebrates: nervous system and sense organs ; VIP</subject><ispartof>Neuroscience, 2008-07, Vol.154 (4), p.1627-1638</ispartof><rights>2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-6f74d6715200dd285cf74317b75cf39a4f17b5823cc22ac17a27db25f111038f3</citedby><cites>FETCH-LOGICAL-c560t-6f74d6715200dd285cf74317b75cf39a4f17b5823cc22ac17a27db25f111038f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuroscience.2008.04.071$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20522578$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18556138$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kabatas, S</creatorcontrib><creatorcontrib>Yu, D</creatorcontrib><creatorcontrib>He, X.D</creatorcontrib><creatorcontrib>Thatte, H.S</creatorcontrib><creatorcontrib>Benedict, D</creatorcontrib><creatorcontrib>Hepgul, K.T</creatorcontrib><creatorcontrib>Black, P.M</creatorcontrib><creatorcontrib>Sabharwal, S</creatorcontrib><creatorcontrib>Teng, Y.D</creatorcontrib><title>Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Abstract Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague–Dawley rats ( n =5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted for 24 h before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (−64.1% and −49.5%) and ileum (−73.6% and −70.1%) at 48 h and 4 weeks p.i., respectively ( P ≤0.005, ANOVA with post hoc t -test). Electrophysiological analysis revealed that purinergic fast inhibitory junction potential (IJP) was reduced ∼30% in the antrum and duodenum of rats 48 h p.i. (numbers of animals/numbers of tissue samples=3/7; P <0.001), and slow IJP was essentially abolished. Immunocytochemistry consequently uncovered significant reductions in the GI vasoactive intestinal polypeptide and neuronal nitric oxide synthase (i.e. slow IJP mediators) reactivity at 48 h and 4 weeks p.i., suggesting that SCI disrupted interstitial neurotransmission. Importantly, SCI caused discernible atrophy of the GI mucosa and muscle coat (e.g. the two layers of gastric wall were correspondingly 28% and 27% thinner 4 weeks p.i.). We conclude that contusive SCI triggers GI abnormalities with unique pathophysiology and pathology in different segments. Such GI disorders evolve continuously during the entire post-SCI period examined, and may require therapeutic development to target specific underlying mechanisms.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastrointestinal Diseases - etiology</subject><subject>Gastrointestinal Diseases - pathology</subject><subject>Gastrointestinal Diseases - physiopathology</subject><subject>gastrointestinal dysfunction</subject><subject>Gastrointestinal Tract - innervation</subject><subject>Gastrointestinal Tract - pathology</subject><subject>Gastrointestinal Tract - physiopathology</subject><subject>Gastrointestinal Transit - physiology</subject><subject>IJP</subject><subject>Immunohistochemistry</subject><subject>Membrane Potentials - physiology</subject><subject>Neurology</subject><subject>Nitric Oxide Synthase Type I - biosynthesis</subject><subject>nNOS</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Spinal Cord Injuries - complications</subject><subject>Spinal Cord Injuries - physiopathology</subject><subject>spinal cord injury</subject><subject>Vasoactive Intestinal Peptide - biosynthesis</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>VIP</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkluL1DAUx4Mo7rj6FaQI-taaa5PxQZD1Cos-qM8hkyZrapuMOakw397UKSq-aCDk5PA7l5x_EHpEcEcw6Z-OXXRLTmCDi9Z1FGPVYd5hSW6hHVGStVJwfhvtMMN9ywWlF-gewIjrEpzdRRdECdETpnYovq-pzNSYONRtSpqDXa-HmPJsplCCgyb5pnxxzY2BklOIxUEJsVJwguLmJjtYpuq5aXxOc2NTLAuEFBs4_sRsykMT4rjk0310x5sJ3IPtvESfX7_6dPW2vf7w5t3Vi-vWih6XtveSD70kor5tGKgStjoYkQdZLbY33FdbKMqspdRYIg2Vw4EKTwjBTHl2iZ6c8x5z-rbUfvUcwLppMtGlBXS_p3vKFf8nSLFilBNawWdn0NbJQ3ZeH3OYTT5pgvUqix71n7LoVRaNua6y1OCHW5XlMLvhd-imQwUeb4CBOn-fTbQBfnEUVxGFXLmXZ87V4X0PLuut3BCys0UPKfxfP8__SmOnEFflv7qTgzEtuQoHmmigGuuP60da_xFWGPeC7NkPpRnJIg</recordid><startdate>20080717</startdate><enddate>20080717</enddate><creator>Kabatas, S</creator><creator>Yu, D</creator><creator>He, X.D</creator><creator>Thatte, H.S</creator><creator>Benedict, D</creator><creator>Hepgul, K.T</creator><creator>Black, P.M</creator><creator>Sabharwal, S</creator><creator>Teng, Y.D</creator><general>Elsevier Ltd</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>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20080717</creationdate><title>Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury</title><author>Kabatas, S ; Yu, D ; He, X.D ; Thatte, H.S ; Benedict, D ; Hepgul, K.T ; Black, P.M ; Sabharwal, S ; Teng, Y.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-6f74d6715200dd285cf74317b75cf39a4f17b5823cc22ac17a27db25f111038f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastrointestinal Diseases - etiology</topic><topic>Gastrointestinal Diseases - pathology</topic><topic>Gastrointestinal Diseases - physiopathology</topic><topic>gastrointestinal dysfunction</topic><topic>Gastrointestinal Tract - innervation</topic><topic>Gastrointestinal Tract - pathology</topic><topic>Gastrointestinal Tract - physiopathology</topic><topic>Gastrointestinal Transit - physiology</topic><topic>IJP</topic><topic>Immunohistochemistry</topic><topic>Membrane Potentials - physiology</topic><topic>Neurology</topic><topic>Nitric Oxide Synthase Type I - biosynthesis</topic><topic>nNOS</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spinal Cord Injuries - complications</topic><topic>Spinal Cord Injuries - physiopathology</topic><topic>spinal cord injury</topic><topic>Vasoactive Intestinal Peptide - biosynthesis</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>VIP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kabatas, S</creatorcontrib><creatorcontrib>Yu, D</creatorcontrib><creatorcontrib>He, X.D</creatorcontrib><creatorcontrib>Thatte, H.S</creatorcontrib><creatorcontrib>Benedict, D</creatorcontrib><creatorcontrib>Hepgul, K.T</creatorcontrib><creatorcontrib>Black, P.M</creatorcontrib><creatorcontrib>Sabharwal, S</creatorcontrib><creatorcontrib>Teng, Y.D</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>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kabatas, S</au><au>Yu, D</au><au>He, X.D</au><au>Thatte, H.S</au><au>Benedict, D</au><au>Hepgul, K.T</au><au>Black, P.M</au><au>Sabharwal, S</au><au>Teng, Y.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2008-07-17</date><risdate>2008</risdate><volume>154</volume><issue>4</issue><spage>1627</spage><epage>1638</epage><pages>1627-1638</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Abstract Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague–Dawley rats ( n =5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted for 24 h before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (−64.1% and −49.5%) and ileum (−73.6% and −70.1%) at 48 h and 4 weeks p.i., respectively ( P ≤0.005, ANOVA with post hoc t -test). Electrophysiological analysis revealed that purinergic fast inhibitory junction potential (IJP) was reduced ∼30% in the antrum and duodenum of rats 48 h p.i. (numbers of animals/numbers of tissue samples=3/7; P <0.001), and slow IJP was essentially abolished. Immunocytochemistry consequently uncovered significant reductions in the GI vasoactive intestinal polypeptide and neuronal nitric oxide synthase (i.e. slow IJP mediators) reactivity at 48 h and 4 weeks p.i., suggesting that SCI disrupted interstitial neurotransmission. Importantly, SCI caused discernible atrophy of the GI mucosa and muscle coat (e.g. the two layers of gastric wall were correspondingly 28% and 27% thinner 4 weeks p.i.). We conclude that contusive SCI triggers GI abnormalities with unique pathophysiology and pathology in different segments. Such GI disorders evolve continuously during the entire post-SCI period examined, and may require therapeutic development to target specific underlying mechanisms.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>18556138</pmid><doi>10.1016/j.neuroscience.2008.04.071</doi><tpages>12</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Female Fundamental and applied biological sciences. Psychology Gastrointestinal Diseases - etiology Gastrointestinal Diseases - pathology Gastrointestinal Diseases - physiopathology gastrointestinal dysfunction Gastrointestinal Tract - innervation Gastrointestinal Tract - pathology Gastrointestinal Tract - physiopathology Gastrointestinal Transit - physiology IJP Immunohistochemistry Membrane Potentials - physiology Neurology Nitric Oxide Synthase Type I - biosynthesis nNOS rat Rats Rats, Sprague-Dawley Spinal Cord Injuries - complications Spinal Cord Injuries - physiopathology spinal cord injury Vasoactive Intestinal Peptide - biosynthesis Vertebrates: nervous system and sense organs VIP |
| title | Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury |
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