Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture
Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-...
Gespeichert in:
Veröffentlicht in: | Molecular neurobiology 2017-12, Vol.54 (10), p.8278-8286 |
---|---|
Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 8286 |
---|---|
container_issue | 10 |
container_start_page | 8278 |
container_title | Molecular neurobiology |
container_volume | 54 |
creator | Zou, Dingquan Luo, Man Han, Zhenying Zhan, Lei Zhu, Wan Kang, Shuai Bao, Chen Li, Zhao Nelson, Jeffrey Zhang, Rui Su, Hua |
description | Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain (
p
= 0.006) and MAO-B-positive astrocytes (
p
|
doi_str_mv | 10.1007/s12035-016-0310-8 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5457363</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1963350463</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</originalsourceid><addsrcrecordid>eNp1kU9v1DAQxS0EokvhA3BBlrhwCdixnTgXpG3VQqUCEn_OljO2G5esvdhO0X57vGypChKnGWne_GaeHkLPKXlNCenfZNoSJhpCu4YwShr5AK2oEENDqWwfohWRA2v6jssj9CTna0LalpL-MTpq-4FyQukK7dZQ_I0uPgYcHV7P20k3Pf7oIRYfPOA12LKbYYqzDxZ_tmC3JabamAVsxidJ-4DPjN1oXJsPHiz-6cuELzJMdlMBX0qK3y3WweCTWBHnSUNZkn2KHjk9Z_vsth6jb-dnX0_fN5ef3l2cri8b4D0pjRt0N3YgwYymVjN0vaN87EfpnHZjC04OpuVMOwKaSTlqzbVkIERnjTOSHaO3B-52GTfWgA0l6Vltk9_otFNRe_X3JPhJXcUbJbjoWccq4NUtIMUfi81FbXwGO8862LhkRSUXknHKRZW-_Ed6HZcUqj1Fh4oShP8G0oMKUsw5WXf3DCVqH6w6BKtqsGofrNq7eHHfxd3GnySroD0Ich2FK5vunf4v9RftiLCM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1963350463</pqid></control><display><type>article</type><title>Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Zou, Dingquan ; Luo, Man ; Han, Zhenying ; Zhan, Lei ; Zhu, Wan ; Kang, Shuai ; Bao, Chen ; Li, Zhao ; Nelson, Jeffrey ; Zhang, Rui ; Su, Hua</creator><creatorcontrib>Zou, Dingquan ; Luo, Man ; Han, Zhenying ; Zhan, Lei ; Zhu, Wan ; Kang, Shuai ; Bao, Chen ; Li, Zhao ; Nelson, Jeffrey ; Zhang, Rui ; Su, Hua</creatorcontrib><description>Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain (
p
= 0.006) and MAO-B-positive astrocytes (
p
< 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice (
p
< 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. Thus, the α-7 nAchR-specific agonist could be developed into a new therapy for improving recovery of patients with stroke or stroke + bone fracture.</description><identifier>ISSN: 0893-7648</identifier><identifier>ISSN: 1559-1182</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-016-0310-8</identifier><identifier>PMID: 27914011</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetylcholine ; Acetylcholine receptors (nicotinic) ; Activation ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Amine oxidase (flavin-containing) ; Animals ; Astrocytes ; Biomedical and Life Sciences ; Biomedicine ; Blood-brain barrier ; Brain Edema - metabolism ; Brain Edema - pathology ; Brain Edema - prevention & control ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain Ischemia - prevention & control ; Cell Biology ; Cerebral blood flow ; Edema ; Fractures ; Fractures, Bone - metabolism ; Fractures, Bone - pathology ; Fractures, Bone - prevention & control ; Ischemia ; Male ; Methyllycaconitine ; Mice ; Mice, Inbred C57BL ; Moisture content ; Neurobiology ; Neurology ; Neurosciences ; Oxidative stress ; Random Allocation ; Risk factors ; Stroke ; Stroke - metabolism ; Stroke - pathology ; Stroke - prevention & control ; Tibia ; Tibia - injuries ; Tibia - metabolism ; Water content ; Water treatment</subject><ispartof>Molecular neurobiology, 2017-12, Vol.54 (10), p.8278-8286</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>Molecular Neurobiology is a copyright of Springer, (2016). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</citedby><cites>FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</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/s12035-016-0310-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-016-0310-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27914011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zou, Dingquan</creatorcontrib><creatorcontrib>Luo, Man</creatorcontrib><creatorcontrib>Han, Zhenying</creatorcontrib><creatorcontrib>Zhan, Lei</creatorcontrib><creatorcontrib>Zhu, Wan</creatorcontrib><creatorcontrib>Kang, Shuai</creatorcontrib><creatorcontrib>Bao, Chen</creatorcontrib><creatorcontrib>Li, Zhao</creatorcontrib><creatorcontrib>Nelson, Jeffrey</creatorcontrib><creatorcontrib>Zhang, Rui</creatorcontrib><creatorcontrib>Su, Hua</creatorcontrib><title>Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain (
p
= 0.006) and MAO-B-positive astrocytes (
p
< 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice (
p
< 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. Thus, the α-7 nAchR-specific agonist could be developed into a new therapy for improving recovery of patients with stroke or stroke + bone fracture.</description><subject>Acetylcholine</subject><subject>Acetylcholine receptors (nicotinic)</subject><subject>Activation</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Amine oxidase (flavin-containing)</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - pathology</subject><subject>Brain Edema - prevention & control</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - prevention & control</subject><subject>Cell Biology</subject><subject>Cerebral blood flow</subject><subject>Edema</subject><subject>Fractures</subject><subject>Fractures, Bone - metabolism</subject><subject>Fractures, Bone - pathology</subject><subject>Fractures, Bone - prevention & control</subject><subject>Ischemia</subject><subject>Male</subject><subject>Methyllycaconitine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Moisture content</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Oxidative stress</subject><subject>Random Allocation</subject><subject>Risk factors</subject><subject>Stroke</subject><subject>Stroke - metabolism</subject><subject>Stroke - pathology</subject><subject>Stroke - prevention & control</subject><subject>Tibia</subject><subject>Tibia - injuries</subject><subject>Tibia - metabolism</subject><subject>Water content</subject><subject>Water treatment</subject><issn>0893-7648</issn><issn>1559-1182</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU9v1DAQxS0EokvhA3BBlrhwCdixnTgXpG3VQqUCEn_OljO2G5esvdhO0X57vGypChKnGWne_GaeHkLPKXlNCenfZNoSJhpCu4YwShr5AK2oEENDqWwfohWRA2v6jssj9CTna0LalpL-MTpq-4FyQukK7dZQ_I0uPgYcHV7P20k3Pf7oIRYfPOA12LKbYYqzDxZ_tmC3JabamAVsxidJ-4DPjN1oXJsPHiz-6cuELzJMdlMBX0qK3y3WweCTWBHnSUNZkn2KHjk9Z_vsth6jb-dnX0_fN5ef3l2cri8b4D0pjRt0N3YgwYymVjN0vaN87EfpnHZjC04OpuVMOwKaSTlqzbVkIERnjTOSHaO3B-52GTfWgA0l6Vltk9_otFNRe_X3JPhJXcUbJbjoWccq4NUtIMUfi81FbXwGO8862LhkRSUXknHKRZW-_Ed6HZcUqj1Fh4oShP8G0oMKUsw5WXf3DCVqH6w6BKtqsGofrNq7eHHfxd3GnySroD0Ich2FK5vunf4v9RftiLCM</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Zou, Dingquan</creator><creator>Luo, Man</creator><creator>Han, Zhenying</creator><creator>Zhan, Lei</creator><creator>Zhu, Wan</creator><creator>Kang, Shuai</creator><creator>Bao, Chen</creator><creator>Li, Zhao</creator><creator>Nelson, Jeffrey</creator><creator>Zhang, Rui</creator><creator>Su, Hua</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>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</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>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171201</creationdate><title>Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture</title><author>Zou, Dingquan ; Luo, Man ; Han, Zhenying ; Zhan, Lei ; Zhu, Wan ; Kang, Shuai ; Bao, Chen ; Li, Zhao ; Nelson, Jeffrey ; Zhang, Rui ; Su, Hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine receptors (nicotinic)</topic><topic>Activation</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Amine oxidase (flavin-containing)</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-brain barrier</topic><topic>Brain Edema - metabolism</topic><topic>Brain Edema - pathology</topic><topic>Brain Edema - prevention & control</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain Ischemia - prevention & control</topic><topic>Cell Biology</topic><topic>Cerebral blood flow</topic><topic>Edema</topic><topic>Fractures</topic><topic>Fractures, Bone - metabolism</topic><topic>Fractures, Bone - pathology</topic><topic>Fractures, Bone - prevention & control</topic><topic>Ischemia</topic><topic>Male</topic><topic>Methyllycaconitine</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Moisture content</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Oxidative stress</topic><topic>Random Allocation</topic><topic>Risk factors</topic><topic>Stroke</topic><topic>Stroke - metabolism</topic><topic>Stroke - pathology</topic><topic>Stroke - prevention & control</topic><topic>Tibia</topic><topic>Tibia - injuries</topic><topic>Tibia - metabolism</topic><topic>Water content</topic><topic>Water treatment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zou, Dingquan</creatorcontrib><creatorcontrib>Luo, Man</creatorcontrib><creatorcontrib>Han, Zhenying</creatorcontrib><creatorcontrib>Zhan, Lei</creatorcontrib><creatorcontrib>Zhu, Wan</creatorcontrib><creatorcontrib>Kang, Shuai</creatorcontrib><creatorcontrib>Bao, Chen</creatorcontrib><creatorcontrib>Li, Zhao</creatorcontrib><creatorcontrib>Nelson, Jeffrey</creatorcontrib><creatorcontrib>Zhang, Rui</creatorcontrib><creatorcontrib>Su, Hua</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>Chemoreception Abstracts</collection><collection>Neurosciences 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>Psychology Database (Alumni)</collection><collection>Science 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>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>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>Psychology Database</collection><collection>Science 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>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zou, Dingquan</au><au>Luo, Man</au><au>Han, Zhenying</au><au>Zhan, Lei</au><au>Zhu, Wan</au><au>Kang, Shuai</au><au>Bao, Chen</au><au>Li, Zhao</au><au>Nelson, Jeffrey</au><au>Zhang, Rui</au><au>Su, Hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>54</volume><issue>10</issue><spage>8278</spage><epage>8286</epage><pages>8278-8286</pages><issn>0893-7648</issn><issn>1559-1182</issn><eissn>1559-1182</eissn><abstract>Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain (
p
= 0.006) and MAO-B-positive astrocytes (
p
< 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice (
p
< 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. Thus, the α-7 nAchR-specific agonist could be developed into a new therapy for improving recovery of patients with stroke or stroke + bone fracture.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27914011</pmid><doi>10.1007/s12035-016-0310-8</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0893-7648 |
ispartof | Molecular neurobiology, 2017-12, Vol.54 (10), p.8278-8286 |
issn | 0893-7648 1559-1182 1559-1182 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5457363 |
source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | Acetylcholine Acetylcholine receptors (nicotinic) Activation alpha7 Nicotinic Acetylcholine Receptor - metabolism Amine oxidase (flavin-containing) Animals Astrocytes Biomedical and Life Sciences Biomedicine Blood-brain barrier Brain Edema - metabolism Brain Edema - pathology Brain Edema - prevention & control Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - prevention & control Cell Biology Cerebral blood flow Edema Fractures Fractures, Bone - metabolism Fractures, Bone - pathology Fractures, Bone - prevention & control Ischemia Male Methyllycaconitine Mice Mice, Inbred C57BL Moisture content Neurobiology Neurology Neurosciences Oxidative stress Random Allocation Risk factors Stroke Stroke - metabolism Stroke - pathology Stroke - prevention & control Tibia Tibia - injuries Tibia - metabolism Water content Water treatment |
title | Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-17T20%3A56%3A46IST&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=Activation%20of%20Alpha-7%20Nicotinic%20Acetylcholine%20Receptor%20Reduces%20Brain%20Edema%20in%20Mice%20with%20Ischemic%20Stroke%20and%20Bone%20Fracture&rft.jtitle=Molecular%20neurobiology&rft.au=Zou,%20Dingquan&rft.date=2017-12-01&rft.volume=54&rft.issue=10&rft.spage=8278&rft.epage=8286&rft.pages=8278-8286&rft.issn=0893-7648&rft.eissn=1559-1182&rft_id=info:doi/10.1007/s12035-016-0310-8&rft_dat=%3Cproquest_pubme%3E1963350463%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=1963350463&rft_id=info:pmid/27914011&rfr_iscdi=true |