Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation
Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmi...
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| Veröffentlicht in: | Scientific reports 2018-01, Vol.8 (1), p.118-118, Article 118 |
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| creator | Chang, Li-Hsin Lin, Hui-Ching Huang, Shiang-Suo Chen, I-Chih Chu, Kai-Wen Chih, Chun-Lien Liang, Yao-Wen Lee, Yi-Chung Chen, You-Yin Lee, Yi-Hsuan Lee, I-Hui |
| description | Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmission and neurotrophic signaling. We used a permanent middle cerebral artery occlusion (MCAO) model in adult wild-type mice with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)dodecanoic acid (AUDA) post-treatment and in sEH knockout (sEH KO) mice. We found that sensorimotor recovery was significantly enhanced after MCAO in both AUDA-treated and sEH KO mice, with decreased sEH activity and brain infarction. Decreased post-ischemic long-term potentiation (iLTP) was observed in an
ex vivo
hippocampal oxygen-glucose deprivation model. Tropomyosin receptor kinase B (TrkB) activation, rather than glutamate receptor alteration, was consistently found after the different manipulations. Immunohistochemistry further revealed peri-infarct neuronal TrkB activation and microvasculature augmentation in AUDA-treated and sEH KO mice, suggesting parallel neurovascular enhancement. Mechanistically, pretreatment with a selective TrkB antagonist ANA12 countered the effect of iLTP attenuation induced by sEH deletion
ex vivo
and abolished the infarct reduction
in vivo
. Together, the neuroprotective effects of sEH inhibition and gene deletion can both be mediated partially via enhancement of TrkB signaling which attenuated post-ischemic neuroexcitation and neurological deficits. |
| doi_str_mv | 10.1038/s41598-017-18558-6 |
| format | Article |
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ex vivo
hippocampal oxygen-glucose deprivation model. Tropomyosin receptor kinase B (TrkB) activation, rather than glutamate receptor alteration, was consistently found after the different manipulations. Immunohistochemistry further revealed peri-infarct neuronal TrkB activation and microvasculature augmentation in AUDA-treated and sEH KO mice, suggesting parallel neurovascular enhancement. Mechanistically, pretreatment with a selective TrkB antagonist ANA12 countered the effect of iLTP attenuation induced by sEH deletion
ex vivo
and abolished the infarct reduction
in vivo
. Together, the neuroprotective effects of sEH inhibition and gene deletion can both be mediated partially via enhancement of TrkB signaling which attenuated post-ischemic neuroexcitation and neurological deficits.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-18558-6</identifier><identifier>PMID: 29311641</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/51 ; 14/19 ; 631/378/1689/534 ; 631/378/2607 ; 64/60 ; 82/80 ; 9/30 ; Animals ; Cerebral blood flow ; Cerebral Cortex - blood supply ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Cerebral infarction ; Disease Models, Animal ; Enzyme Activation ; Epoxide hydrolase ; Epoxide Hydrolases - antagonists & inhibitors ; Epoxide Hydrolases - deficiency ; Excitatory Postsynaptic Potentials ; Gene Deletion ; Glucose ; Glutamic acid receptors ; Hippocampus ; Hippocampus - metabolism ; Humanities and Social Sciences ; Immunohistochemistry ; Ischemia ; Long-term potentiation ; Male ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Knockout ; Microvasculature ; Motor Activity ; multidisciplinary ; Neurological diseases ; Neurons - metabolism ; Neuroprotection ; Neuroprotective Agents ; Oxygen ; Protein-Tyrosine Kinases - metabolism ; Psychomotor Performance ; Rodents ; Science ; Science (multidisciplinary) ; Sensorimotor system ; Staphylococcal enterotoxin H ; Stroke ; Stroke - etiology ; Stroke - metabolism ; Stroke - physiopathology ; Synaptic Transmission ; TrkB receptors ; Tropomyosin ; Vasoactive agents</subject><ispartof>Scientific reports, 2018-01, Vol.8 (1), p.118-118, Article 118</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-9d9c7d3165f15aa8bd379b8e1a8830b63e726ea1786c38c378049aeb2f648a303</citedby><cites>FETCH-LOGICAL-c474t-9d9c7d3165f15aa8bd379b8e1a8830b63e726ea1786c38c378049aeb2f648a303</cites><orcidid>0000-0002-5344-6685</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5758800/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5758800/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29311641$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Li-Hsin</creatorcontrib><creatorcontrib>Lin, Hui-Ching</creatorcontrib><creatorcontrib>Huang, Shiang-Suo</creatorcontrib><creatorcontrib>Chen, I-Chih</creatorcontrib><creatorcontrib>Chu, Kai-Wen</creatorcontrib><creatorcontrib>Chih, Chun-Lien</creatorcontrib><creatorcontrib>Liang, Yao-Wen</creatorcontrib><creatorcontrib>Lee, Yi-Chung</creatorcontrib><creatorcontrib>Chen, You-Yin</creatorcontrib><creatorcontrib>Lee, Yi-Hsuan</creatorcontrib><creatorcontrib>Lee, I-Hui</creatorcontrib><title>Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmission and neurotrophic signaling. We used a permanent middle cerebral artery occlusion (MCAO) model in adult wild-type mice with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)dodecanoic acid (AUDA) post-treatment and in sEH knockout (sEH KO) mice. We found that sensorimotor recovery was significantly enhanced after MCAO in both AUDA-treated and sEH KO mice, with decreased sEH activity and brain infarction. Decreased post-ischemic long-term potentiation (iLTP) was observed in an
ex vivo
hippocampal oxygen-glucose deprivation model. Tropomyosin receptor kinase B (TrkB) activation, rather than glutamate receptor alteration, was consistently found after the different manipulations. Immunohistochemistry further revealed peri-infarct neuronal TrkB activation and microvasculature augmentation in AUDA-treated and sEH KO mice, suggesting parallel neurovascular enhancement. Mechanistically, pretreatment with a selective TrkB antagonist ANA12 countered the effect of iLTP attenuation induced by sEH deletion
ex vivo
and abolished the infarct reduction
in vivo
. Together, the neuroprotective effects of sEH inhibition and gene deletion can both be mediated partially via enhancement of TrkB signaling which attenuated post-ischemic neuroexcitation and neurological deficits.</description><subject>13/1</subject><subject>13/51</subject><subject>14/19</subject><subject>631/378/1689/534</subject><subject>631/378/2607</subject><subject>64/60</subject><subject>82/80</subject><subject>9/30</subject><subject>Animals</subject><subject>Cerebral blood flow</subject><subject>Cerebral Cortex - blood supply</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral infarction</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation</subject><subject>Epoxide hydrolase</subject><subject>Epoxide Hydrolases - antagonists & inhibitors</subject><subject>Epoxide Hydrolases - deficiency</subject><subject>Excitatory Postsynaptic Potentials</subject><subject>Gene Deletion</subject><subject>Glucose</subject><subject>Glutamic acid receptors</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Humanities and Social Sciences</subject><subject>Immunohistochemistry</subject><subject>Ischemia</subject><subject>Long-term potentiation</subject><subject>Male</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microvasculature</subject><subject>Motor Activity</subject><subject>multidisciplinary</subject><subject>Neurological diseases</subject><subject>Neurons - metabolism</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents</subject><subject>Oxygen</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Psychomotor Performance</subject><subject>Rodents</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Sensorimotor system</subject><subject>Staphylococcal enterotoxin H</subject><subject>Stroke</subject><subject>Stroke - etiology</subject><subject>Stroke - metabolism</subject><subject>Stroke - physiopathology</subject><subject>Synaptic Transmission</subject><subject>TrkB receptors</subject><subject>Tropomyosin</subject><subject>Vasoactive agents</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp1kc1u1DAUhSMEolXpC7BAltiwCfVvYm-QaMVPpUpsytpynJsZdzx2sJ3SvgZPjKdTqgEJb2z5fudc-56meU3we4KZPMucCCVbTPqWSCFk2z1rjinmoqWM0ucH56PmNOcbXJegihP1sjmiihHScXLc_Dr30W7MCChOKEe_DB4QzPHO1av1_ZiiNxmQKQXCYgpkNMdcWpftGrbOogBLisH4ys6Q4M66YoqLAZkwIhvDBCmjBNl5B8FWo5VxIReUS4obQD9dWaPrtDlHxhZ3-yB91byYjM9w-rifNN8_f7q--NpefftyefHxqrW856VVo7L9yEgnJiKMkcPIejVIIEZKhoeOQU87MKSXnWXSsl5irgwMdOq4NAyzk-bD3ndehi2MFkJJxus5ua1J9zoap_-uBLfWq3irRS-kxDuDd48GKf5YIBe9rXMB702AuGRNlFRCcKZURd_-g97EJdW57SjFOOkxoZWie8qmmHOC6ekxBOtd6nqfuq6p64fUdVdFbw6_8ST5k3EF2B7ItRRWkA56_9_2N5NgvEo</recordid><startdate>20180108</startdate><enddate>20180108</enddate><creator>Chang, Li-Hsin</creator><creator>Lin, Hui-Ching</creator><creator>Huang, Shiang-Suo</creator><creator>Chen, I-Chih</creator><creator>Chu, Kai-Wen</creator><creator>Chih, Chun-Lien</creator><creator>Liang, Yao-Wen</creator><creator>Lee, Yi-Chung</creator><creator>Chen, You-Yin</creator><creator>Lee, Yi-Hsuan</creator><creator>Lee, I-Hui</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5344-6685</orcidid></search><sort><creationdate>20180108</creationdate><title>Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation</title><author>Chang, Li-Hsin ; Lin, Hui-Ching ; Huang, Shiang-Suo ; Chen, I-Chih ; Chu, Kai-Wen ; Chih, Chun-Lien ; Liang, Yao-Wen ; Lee, Yi-Chung ; Chen, You-Yin ; Lee, Yi-Hsuan ; Lee, I-Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-9d9c7d3165f15aa8bd379b8e1a8830b63e726ea1786c38c378049aeb2f648a303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13/1</topic><topic>13/51</topic><topic>14/19</topic><topic>631/378/1689/534</topic><topic>631/378/2607</topic><topic>64/60</topic><topic>82/80</topic><topic>9/30</topic><topic>Animals</topic><topic>Cerebral blood flow</topic><topic>Cerebral Cortex - blood supply</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral infarction</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation</topic><topic>Epoxide hydrolase</topic><topic>Epoxide Hydrolases - antagonists & inhibitors</topic><topic>Epoxide Hydrolases - deficiency</topic><topic>Excitatory Postsynaptic Potentials</topic><topic>Gene Deletion</topic><topic>Glucose</topic><topic>Glutamic acid receptors</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Humanities and Social Sciences</topic><topic>Immunohistochemistry</topic><topic>Ischemia</topic><topic>Long-term potentiation</topic><topic>Male</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microvasculature</topic><topic>Motor Activity</topic><topic>multidisciplinary</topic><topic>Neurological diseases</topic><topic>Neurons - metabolism</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents</topic><topic>Oxygen</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Psychomotor Performance</topic><topic>Rodents</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Sensorimotor system</topic><topic>Staphylococcal enterotoxin H</topic><topic>Stroke</topic><topic>Stroke - etiology</topic><topic>Stroke - metabolism</topic><topic>Stroke - physiopathology</topic><topic>Synaptic Transmission</topic><topic>TrkB receptors</topic><topic>Tropomyosin</topic><topic>Vasoactive agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Li-Hsin</creatorcontrib><creatorcontrib>Lin, Hui-Ching</creatorcontrib><creatorcontrib>Huang, Shiang-Suo</creatorcontrib><creatorcontrib>Chen, I-Chih</creatorcontrib><creatorcontrib>Chu, Kai-Wen</creatorcontrib><creatorcontrib>Chih, Chun-Lien</creatorcontrib><creatorcontrib>Liang, Yao-Wen</creatorcontrib><creatorcontrib>Lee, Yi-Chung</creatorcontrib><creatorcontrib>Chen, You-Yin</creatorcontrib><creatorcontrib>Lee, Yi-Hsuan</creatorcontrib><creatorcontrib>Lee, I-Hui</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>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>Science Database (Alumni Edition)</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 One Sustainability</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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Li-Hsin</au><au>Lin, Hui-Ching</au><au>Huang, Shiang-Suo</au><au>Chen, I-Chih</au><au>Chu, Kai-Wen</au><au>Chih, Chun-Lien</au><au>Liang, Yao-Wen</au><au>Lee, Yi-Chung</au><au>Chen, You-Yin</au><au>Lee, Yi-Hsuan</au><au>Lee, I-Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-01-08</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>118</spage><epage>118</epage><pages>118-118</pages><artnum>118</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmission and neurotrophic signaling. We used a permanent middle cerebral artery occlusion (MCAO) model in adult wild-type mice with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)dodecanoic acid (AUDA) post-treatment and in sEH knockout (sEH KO) mice. We found that sensorimotor recovery was significantly enhanced after MCAO in both AUDA-treated and sEH KO mice, with decreased sEH activity and brain infarction. Decreased post-ischemic long-term potentiation (iLTP) was observed in an
ex vivo
hippocampal oxygen-glucose deprivation model. Tropomyosin receptor kinase B (TrkB) activation, rather than glutamate receptor alteration, was consistently found after the different manipulations. Immunohistochemistry further revealed peri-infarct neuronal TrkB activation and microvasculature augmentation in AUDA-treated and sEH KO mice, suggesting parallel neurovascular enhancement. Mechanistically, pretreatment with a selective TrkB antagonist ANA12 countered the effect of iLTP attenuation induced by sEH deletion
ex vivo
and abolished the infarct reduction
in vivo
. Together, the neuroprotective effects of sEH inhibition and gene deletion can both be mediated partially via enhancement of TrkB signaling which attenuated post-ischemic neuroexcitation and neurological deficits.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29311641</pmid><doi>10.1038/s41598-017-18558-6</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5344-6685</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Scientific reports, 2018-01, Vol.8 (1), p.118-118, Article 118 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5758800 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 13/1 13/51 14/19 631/378/1689/534 631/378/2607 64/60 82/80 9/30 Animals Cerebral blood flow Cerebral Cortex - blood supply Cerebral Cortex - metabolism Cerebral Cortex - pathology Cerebral infarction Disease Models, Animal Enzyme Activation Epoxide hydrolase Epoxide Hydrolases - antagonists & inhibitors Epoxide Hydrolases - deficiency Excitatory Postsynaptic Potentials Gene Deletion Glucose Glutamic acid receptors Hippocampus Hippocampus - metabolism Humanities and Social Sciences Immunohistochemistry Ischemia Long-term potentiation Male Membrane Glycoproteins - metabolism Mice Mice, Knockout Microvasculature Motor Activity multidisciplinary Neurological diseases Neurons - metabolism Neuroprotection Neuroprotective Agents Oxygen Protein-Tyrosine Kinases - metabolism Psychomotor Performance Rodents Science Science (multidisciplinary) Sensorimotor system Staphylococcal enterotoxin H Stroke Stroke - etiology Stroke - metabolism Stroke - physiopathology Synaptic Transmission TrkB receptors Tropomyosin Vasoactive agents |
| title | Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T23%3A38%3A39IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Blockade%20of%20soluble%20epoxide%20hydrolase%20attenuates%20post-ischemic%20neuronal%20hyperexcitation%20and%20confers%20resilience%20against%20stroke%20with%20TrkB%20activation&rft.jtitle=Scientific%20reports&rft.au=Chang,%20Li-Hsin&rft.date=2018-01-08&rft.volume=8&rft.issue=1&rft.spage=118&rft.epage=118&rft.pages=118-118&rft.artnum=118&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-017-18558-6&rft_dat=%3Cproquest_pubme%3E1989554399%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1993417012&rft_id=info:pmid/29311641&rfr_iscdi=true |