Massive accumulation of N‐acylethanolamines after stroke. Cell signalling in acute cerebral ischemia?
We investigated levels and compositions of N‐acylethanolamines (NAEs) and their precursors, N‐acyl phosphatidylethanolamines (N‐acyl PEs), in a rat stroke model applying striatal microdialysis for glutamate assay. Rats (n = 18) were treated with either intravenous saline (control), NMDA receptor ant...
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| Veröffentlicht in: | Journal of neurochemistry 2004-03, Vol.88 (5), p.1159-1167 |
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| creator | Berger, Christian Schmid, Patricia C. Schabitz, Wolf‐Ruediger Wolf, Margit Schwab, Stefan Schmid, Harald H. O. |
| description | We investigated levels and compositions of N‐acylethanolamines (NAEs) and their precursors, N‐acyl phosphatidylethanolamines (N‐acyl PEs), in a rat stroke model applying striatal microdialysis for glutamate assay. Rats (n = 18) were treated with either intravenous saline (control), NMDA receptor antagonist MK801 (1 mg/kg), or CB1 receptor antagonist SR141716A (1 mg/kg) 30 min after permanent middle cerebral artery occlusion (MCAO). MK801 significantly attenuated the release of glutamate in the infarcted striatum (79 ± 22 μmol/L) as compared with controls (322 ± 104 μmol/L). The administration of CB1 antagonist SR141716A had no statistically significant effect on glutamate release (340 ± 89 μmol/L), but reduced infarct volume at 5 h after MCAO significantly by approximately 40%, whereas MK801 treatment resulted in a non‐significant (18%) reduction of infarct volume. In controls, striatal and cortical NAE concentrations were about 30‐fold higher in the infarcted than in the non‐infarcted hemisphere, whereas ipsilateral N‐acyl phosphatidylethanolamine (N‐acyl PE) levels exceeded contralateral levels by only a factor of two to three. Treatment with MK801 or SR141716A, or glutamate release in the infarcted tissue, had no significant effect on these levels. NAE accumulation during acute stroke may be due to increased synthesis as well as decreased degradation, possibly by inhibition of fatty acid amide hydrolase (FAAH). |
| doi_str_mv | 10.1046/j.1471-4159.2003.02244.x |
| format | Article |
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Cell signalling in acute cerebral ischemia?</title><source>Wiley Free Content</source><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Berger, Christian ; Schmid, Patricia C. ; Schabitz, Wolf‐Ruediger ; Wolf, Margit ; Schwab, Stefan ; Schmid, Harald H. O.</creator><creatorcontrib>Berger, Christian ; Schmid, Patricia C. ; Schabitz, Wolf‐Ruediger ; Wolf, Margit ; Schwab, Stefan ; Schmid, Harald H. O.</creatorcontrib><description>We investigated levels and compositions of N‐acylethanolamines (NAEs) and their precursors, N‐acyl phosphatidylethanolamines (N‐acyl PEs), in a rat stroke model applying striatal microdialysis for glutamate assay. Rats (n = 18) were treated with either intravenous saline (control), NMDA receptor antagonist MK801 (1 mg/kg), or CB1 receptor antagonist SR141716A (1 mg/kg) 30 min after permanent middle cerebral artery occlusion (MCAO). MK801 significantly attenuated the release of glutamate in the infarcted striatum (79 ± 22 μmol/L) as compared with controls (322 ± 104 μmol/L). The administration of CB1 antagonist SR141716A had no statistically significant effect on glutamate release (340 ± 89 μmol/L), but reduced infarct volume at 5 h after MCAO significantly by approximately 40%, whereas MK801 treatment resulted in a non‐significant (18%) reduction of infarct volume. In controls, striatal and cortical NAE concentrations were about 30‐fold higher in the infarcted than in the non‐infarcted hemisphere, whereas ipsilateral N‐acyl phosphatidylethanolamine (N‐acyl PE) levels exceeded contralateral levels by only a factor of two to three. Treatment with MK801 or SR141716A, or glutamate release in the infarcted tissue, had no significant effect on these levels. NAE accumulation during acute stroke may be due to increased synthesis as well as decreased degradation, possibly by inhibition of fatty acid amide hydrolase (FAAH).</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.2003.02244.x</identifier><identifier>PMID: 15009671</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Acute Disease ; Animals ; Arachidonic Acids - metabolism ; Biological and medical sciences ; Brain Ischemia - metabolism ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Disease Models, Animal ; Dizocilpine Maleate - pharmacology ; Endocannabinoids ; Ethanolamines - metabolism ; Excitatory Amino Acid Antagonists - pharmacology ; Extracellular Fluid - metabolism ; glutamate ; ischemic stroke ; Male ; Medical sciences ; Microdialysis ; Neurology ; N‐acylethanolamines ; Phospholipids - metabolism ; Piperidines - pharmacology ; Polyunsaturated Alkamides ; Pyrazoles - pharmacology ; Rats ; Rats, Wistar ; Receptor, Cannabinoid, CB1 - antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors ; Rimonabant ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Stroke - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of neurochemistry, 2004-03, Vol.88 (5), p.1159-1167</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4454-2eb3c88f263c6af60293700e1326d280fce6445640d9e8ccb18acc7dd236af23</citedby><cites>FETCH-LOGICAL-c4454-2eb3c88f263c6af60293700e1326d280fce6445640d9e8ccb18acc7dd236af23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.2003.02244.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.2003.02244.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15532161$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15009671$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berger, Christian</creatorcontrib><creatorcontrib>Schmid, Patricia C.</creatorcontrib><creatorcontrib>Schabitz, Wolf‐Ruediger</creatorcontrib><creatorcontrib>Wolf, Margit</creatorcontrib><creatorcontrib>Schwab, Stefan</creatorcontrib><creatorcontrib>Schmid, Harald H. O.</creatorcontrib><title>Massive accumulation of N‐acylethanolamines after stroke. Cell signalling in acute cerebral ischemia?</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>We investigated levels and compositions of N‐acylethanolamines (NAEs) and their precursors, N‐acyl phosphatidylethanolamines (N‐acyl PEs), in a rat stroke model applying striatal microdialysis for glutamate assay. Rats (n = 18) were treated with either intravenous saline (control), NMDA receptor antagonist MK801 (1 mg/kg), or CB1 receptor antagonist SR141716A (1 mg/kg) 30 min after permanent middle cerebral artery occlusion (MCAO). MK801 significantly attenuated the release of glutamate in the infarcted striatum (79 ± 22 μmol/L) as compared with controls (322 ± 104 μmol/L). The administration of CB1 antagonist SR141716A had no statistically significant effect on glutamate release (340 ± 89 μmol/L), but reduced infarct volume at 5 h after MCAO significantly by approximately 40%, whereas MK801 treatment resulted in a non‐significant (18%) reduction of infarct volume. In controls, striatal and cortical NAE concentrations were about 30‐fold higher in the infarcted than in the non‐infarcted hemisphere, whereas ipsilateral N‐acyl phosphatidylethanolamine (N‐acyl PE) levels exceeded contralateral levels by only a factor of two to three. Treatment with MK801 or SR141716A, or glutamate release in the infarcted tissue, had no significant effect on these levels. NAE accumulation during acute stroke may be due to increased synthesis as well as decreased degradation, possibly by inhibition of fatty acid amide hydrolase (FAAH).</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Arachidonic Acids - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - metabolism</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dizocilpine Maleate - pharmacology</subject><subject>Endocannabinoids</subject><subject>Ethanolamines - metabolism</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Extracellular Fluid - metabolism</subject><subject>glutamate</subject><subject>ischemic stroke</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microdialysis</subject><subject>Neurology</subject><subject>N‐acylethanolamines</subject><subject>Phospholipids - metabolism</subject><subject>Piperidines - pharmacology</subject><subject>Polyunsaturated Alkamides</subject><subject>Pyrazoles - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</subject><subject>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</subject><subject>Rimonabant</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Stroke - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkM1u1DAQxy1ERZfCKyBf4JYw_lgne0AIrfhUKZferVlnsvXiJMVOSvfGI_CMfZI67KpwRD6M5fnN-K8fY1xAKUCb17tS6EoUWixXpQRQJUipdXn7iC0eGo_ZAvJzoUDLU_Y0pR2AMNqIJ-xULAFWphILtv2KKfkb4ujc1E0BRz_0fGj5xd2v3-j2gcYr7IeAne8pcWxHijyNcfhOJV9TCDz5bY8h-H7LfZ_XTCNxR5E2EQP3yV1R5_HtM3bSYkj0_FjP2OWH95frT8X5t4-f1-_OC6f1UheSNsrVdSuNcgZbA3KlKgASSppG1tA6Mhk0GpoV1c5tRJ2DV00jVcalOmOvDmuv4_BjojTaLkfIMbGnYUq2EvmArjJYH0AXh5QitfY6-g7j3gqws2O7s7NKO6u0s2P7x7G9zaMvjn9Mm46av4NHqRl4eQQwOQxtxN759A-3VFKYmXtz4H76QPv_DmC_XKznm7oHPOaZLQ</recordid><startdate>200403</startdate><enddate>200403</enddate><creator>Berger, Christian</creator><creator>Schmid, Patricia C.</creator><creator>Schabitz, Wolf‐Ruediger</creator><creator>Wolf, Margit</creator><creator>Schwab, Stefan</creator><creator>Schmid, Harald H. O.</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>200403</creationdate><title>Massive accumulation of N‐acylethanolamines after stroke. Cell signalling in acute cerebral ischemia?</title><author>Berger, Christian ; Schmid, Patricia C. ; Schabitz, Wolf‐Ruediger ; Wolf, Margit ; Schwab, Stefan ; Schmid, Harald H. O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4454-2eb3c88f263c6af60293700e1326d280fce6445640d9e8ccb18acc7dd236af23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Arachidonic Acids - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - metabolism</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Disease Models, Animal</topic><topic>Dizocilpine Maleate - pharmacology</topic><topic>Endocannabinoids</topic><topic>Ethanolamines - metabolism</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Extracellular Fluid - metabolism</topic><topic>glutamate</topic><topic>ischemic stroke</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microdialysis</topic><topic>Neurology</topic><topic>N‐acylethanolamines</topic><topic>Phospholipids - metabolism</topic><topic>Piperidines - pharmacology</topic><topic>Polyunsaturated Alkamides</topic><topic>Pyrazoles - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</topic><topic>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</topic><topic>Rimonabant</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Stroke - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Berger, Christian</creatorcontrib><creatorcontrib>Schmid, Patricia C.</creatorcontrib><creatorcontrib>Schabitz, Wolf‐Ruediger</creatorcontrib><creatorcontrib>Wolf, Margit</creatorcontrib><creatorcontrib>Schwab, Stefan</creatorcontrib><creatorcontrib>Schmid, Harald H. O.</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>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Berger, Christian</au><au>Schmid, Patricia C.</au><au>Schabitz, Wolf‐Ruediger</au><au>Wolf, Margit</au><au>Schwab, Stefan</au><au>Schmid, Harald H. O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Massive accumulation of N‐acylethanolamines after stroke. Cell signalling in acute cerebral ischemia?</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2004-03</date><risdate>2004</risdate><volume>88</volume><issue>5</issue><spage>1159</spage><epage>1167</epage><pages>1159-1167</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>We investigated levels and compositions of N‐acylethanolamines (NAEs) and their precursors, N‐acyl phosphatidylethanolamines (N‐acyl PEs), in a rat stroke model applying striatal microdialysis for glutamate assay. Rats (n = 18) were treated with either intravenous saline (control), NMDA receptor antagonist MK801 (1 mg/kg), or CB1 receptor antagonist SR141716A (1 mg/kg) 30 min after permanent middle cerebral artery occlusion (MCAO). MK801 significantly attenuated the release of glutamate in the infarcted striatum (79 ± 22 μmol/L) as compared with controls (322 ± 104 μmol/L). The administration of CB1 antagonist SR141716A had no statistically significant effect on glutamate release (340 ± 89 μmol/L), but reduced infarct volume at 5 h after MCAO significantly by approximately 40%, whereas MK801 treatment resulted in a non‐significant (18%) reduction of infarct volume. In controls, striatal and cortical NAE concentrations were about 30‐fold higher in the infarcted than in the non‐infarcted hemisphere, whereas ipsilateral N‐acyl phosphatidylethanolamine (N‐acyl PE) levels exceeded contralateral levels by only a factor of two to three. Treatment with MK801 or SR141716A, or glutamate release in the infarcted tissue, had no significant effect on these levels. NAE accumulation during acute stroke may be due to increased synthesis as well as decreased degradation, possibly by inhibition of fatty acid amide hydrolase (FAAH).</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15009671</pmid><doi>10.1046/j.1471-4159.2003.02244.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Animals Arachidonic Acids - metabolism Biological and medical sciences Brain Ischemia - metabolism Cerebral Cortex - drug effects Cerebral Cortex - metabolism Corpus Striatum - drug effects Corpus Striatum - metabolism Disease Models, Animal Dizocilpine Maleate - pharmacology Endocannabinoids Ethanolamines - metabolism Excitatory Amino Acid Antagonists - pharmacology Extracellular Fluid - metabolism glutamate ischemic stroke Male Medical sciences Microdialysis Neurology N‐acylethanolamines Phospholipids - metabolism Piperidines - pharmacology Polyunsaturated Alkamides Pyrazoles - pharmacology Rats Rats, Wistar Receptor, Cannabinoid, CB1 - antagonists & inhibitors Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Rimonabant Signal Transduction - drug effects Signal Transduction - physiology Stroke - metabolism Vascular diseases and vascular malformations of the nervous system |
| title | Massive accumulation of N‐acylethanolamines after stroke. Cell signalling in acute cerebral ischemia? |
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