Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis‐associated encephalopathy
Background Patients with sepsis‐associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE. Methods The...
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| Veröffentlicht in: | CNS neuroscience & therapeutics 2024-03, Vol.30 (3), p.e14655-n/a |
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| description | Background
Patients with sepsis‐associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE.
Methods
The mouse models of SAE were established by injection of lipopolysaccharide (LPS, 10 mg/kg, intraperitoneal) and cecal ligation puncture (CLP) respectively. Barnes maze, new object recognition test and open field test were used to evaluate the effects of fluoxetine (selective serotonin reuptake inhibitor) and cyproheptadine (nonselective 5‐HT2 receptor antagonist) on cognition and motor activity of mice. Additionally, WAY100635 (5‐HT1A receptor antagonist) was co‐administered with fluoxetine to explore the mechanism underlying effect of fluoxetine on cognitive impairments of SAE. Enzyme‐linked immunosorbent assay (ELISA) was performed to determine 5‐HT levels in hippocampus, brainstem and frontal lobe of experimental groups.
Results
Both LPS‐induced sepsis and CLP induced sepsis resulted in a notable learning deficit. Fluoxetine ameliorated, while cyproheptadine aggravated, cognitive impairment in two classic mouse models of SAE. The cognition‐enhancing effect of fluoxetine is reversed by WAY100635. Decreased 5‐HT levels in hippocampus, brainstem and frontal lobe were observed in LPS septic model and CLP septic model. Notably, both fluoxetine and cyproheptadine significantly increased 5‐HT levels in those brain regions in LPS septic model. Additionally, fluoxetine significantly increased 5‐HT levels in frontal lobe of CLP septic model.
Conclusions
Our study demonstrated that serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. These findings contribute to identification of novel targets to prevent and arrest cognitive impairment in SAE.
Septic mice exhibited cognitive dysfunction and decreased 5‐HT in brain region associated with cognition, and cognitive performance was mediated by SSRI and 5‐HT receptor antagonist. Serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. |
| doi_str_mv | 10.1111/cns.14655 |
| format | Article |
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Patients with sepsis‐associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE.
Methods
The mouse models of SAE were established by injection of lipopolysaccharide (LPS, 10 mg/kg, intraperitoneal) and cecal ligation puncture (CLP) respectively. Barnes maze, new object recognition test and open field test were used to evaluate the effects of fluoxetine (selective serotonin reuptake inhibitor) and cyproheptadine (nonselective 5‐HT2 receptor antagonist) on cognition and motor activity of mice. Additionally, WAY100635 (5‐HT1A receptor antagonist) was co‐administered with fluoxetine to explore the mechanism underlying effect of fluoxetine on cognitive impairments of SAE. Enzyme‐linked immunosorbent assay (ELISA) was performed to determine 5‐HT levels in hippocampus, brainstem and frontal lobe of experimental groups.
Results
Both LPS‐induced sepsis and CLP induced sepsis resulted in a notable learning deficit. Fluoxetine ameliorated, while cyproheptadine aggravated, cognitive impairment in two classic mouse models of SAE. The cognition‐enhancing effect of fluoxetine is reversed by WAY100635. Decreased 5‐HT levels in hippocampus, brainstem and frontal lobe were observed in LPS septic model and CLP septic model. Notably, both fluoxetine and cyproheptadine significantly increased 5‐HT levels in those brain regions in LPS septic model. Additionally, fluoxetine significantly increased 5‐HT levels in frontal lobe of CLP septic model.
Conclusions
Our study demonstrated that serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. These findings contribute to identification of novel targets to prevent and arrest cognitive impairment in SAE.
Septic mice exhibited cognitive dysfunction and decreased 5‐HT in brain region associated with cognition, and cognitive performance was mediated by SSRI and 5‐HT receptor antagonist. Serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE.</description><identifier>ISSN: 1755-5930</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.14655</identifier><identifier>PMID: 38433019</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Abdomen ; Analysis ; Animal cognition ; Animal models ; Animals ; Brain stem ; Cecum ; Cognition ; Cognition disorders ; Cognitive ability ; cognitive dysfunction ; Cognitive Dysfunction - drug therapy ; Cognitive Dysfunction - etiology ; Cyproheptadine ; Cyproheptadine - pharmacology ; Cyproheptadine - therapeutic use ; Disease Models, Animal ; Encephalopathy ; Enzyme-linked immunosorbent assay ; Enzymes ; Fluoxetine ; Fluoxetine - pharmacology ; Fluoxetine - therapeutic use ; Frontal lobe ; Hippocampus ; Humans ; Infection ; Laboratory animals ; Lipopolysaccharides ; Lipopolysaccharides - toxicity ; Medical prognosis ; Memory ; Mice ; Motor activity ; Neurotransmission ; Open-field behavior ; Original ; Pattern recognition ; Sepsis ; Sepsis - complications ; Sepsis-Associated Encephalopathy - complications ; sepsis‐associated encephalopathy ; serotonergic neurotransmission ; Serotonin ; Serotonin S1 receptors ; Serotonin S2 receptors ; Serotonin uptake inhibitors ; therapeutics</subject><ispartof>CNS neuroscience & therapeutics, 2024-03, Vol.30 (3), p.e14655-n/a</ispartof><rights>2024 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2024 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.</rights><rights>COPYRIGHT 2024 John Wiley & Sons, Inc.</rights><rights>2024. 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><cites>FETCH-LOGICAL-c4715-97231b27fd91fbd89e74806e52e0c53db46e68807931fefba364c834c335a0193</cites><orcidid>0000-0002-3758-7824</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/PMC10909618/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10909618/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38433019$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Chen</creatorcontrib><creatorcontrib>Tian, Fafa</creatorcontrib><creatorcontrib>Peng, Jing</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Li, Jingchen</creatorcontrib><creatorcontrib>Zhang, Lina</creatorcontrib><creatorcontrib>Tan, Zheren</creatorcontrib><title>Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis‐associated encephalopathy</title><title>CNS neuroscience & therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>Background
Patients with sepsis‐associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE.
Methods
The mouse models of SAE were established by injection of lipopolysaccharide (LPS, 10 mg/kg, intraperitoneal) and cecal ligation puncture (CLP) respectively. Barnes maze, new object recognition test and open field test were used to evaluate the effects of fluoxetine (selective serotonin reuptake inhibitor) and cyproheptadine (nonselective 5‐HT2 receptor antagonist) on cognition and motor activity of mice. Additionally, WAY100635 (5‐HT1A receptor antagonist) was co‐administered with fluoxetine to explore the mechanism underlying effect of fluoxetine on cognitive impairments of SAE. Enzyme‐linked immunosorbent assay (ELISA) was performed to determine 5‐HT levels in hippocampus, brainstem and frontal lobe of experimental groups.
Results
Both LPS‐induced sepsis and CLP induced sepsis resulted in a notable learning deficit. Fluoxetine ameliorated, while cyproheptadine aggravated, cognitive impairment in two classic mouse models of SAE. The cognition‐enhancing effect of fluoxetine is reversed by WAY100635. Decreased 5‐HT levels in hippocampus, brainstem and frontal lobe were observed in LPS septic model and CLP septic model. Notably, both fluoxetine and cyproheptadine significantly increased 5‐HT levels in those brain regions in LPS septic model. Additionally, fluoxetine significantly increased 5‐HT levels in frontal lobe of CLP septic model.
Conclusions
Our study demonstrated that serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. These findings contribute to identification of novel targets to prevent and arrest cognitive impairment in SAE.
Septic mice exhibited cognitive dysfunction and decreased 5‐HT in brain region associated with cognition, and cognitive performance was mediated by SSRI and 5‐HT receptor antagonist. Serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE.</description><subject>Abdomen</subject><subject>Analysis</subject><subject>Animal cognition</subject><subject>Animal models</subject><subject>Animals</subject><subject>Brain stem</subject><subject>Cecum</subject><subject>Cognition</subject><subject>Cognition disorders</subject><subject>Cognitive ability</subject><subject>cognitive dysfunction</subject><subject>Cognitive Dysfunction - drug therapy</subject><subject>Cognitive Dysfunction - etiology</subject><subject>Cyproheptadine</subject><subject>Cyproheptadine - pharmacology</subject><subject>Cyproheptadine - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Encephalopathy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Enzymes</subject><subject>Fluoxetine</subject><subject>Fluoxetine - pharmacology</subject><subject>Fluoxetine - therapeutic use</subject><subject>Frontal lobe</subject><subject>Hippocampus</subject><subject>Humans</subject><subject>Infection</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Medical prognosis</subject><subject>Memory</subject><subject>Mice</subject><subject>Motor activity</subject><subject>Neurotransmission</subject><subject>Open-field behavior</subject><subject>Original</subject><subject>Pattern recognition</subject><subject>Sepsis</subject><subject>Sepsis - complications</subject><subject>Sepsis-Associated Encephalopathy - complications</subject><subject>sepsis‐associated encephalopathy</subject><subject>serotonergic neurotransmission</subject><subject>Serotonin</subject><subject>Serotonin S1 receptors</subject><subject>Serotonin S2 receptors</subject><subject>Serotonin uptake inhibitors</subject><subject>therapeutics</subject><issn>1755-5930</issn><issn>1755-5949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</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>eNp1Us1u1DAQjhAVLYUDL4AicWkPu7XjOLZPqFpRQKrgUDhbjjPedZXYIU662huP0GfskzBL2hUgYcu_881nfzOTZW8oWVJsFzakJS0rzp9lJ1RwvuCqVM8Pe0aOs5cp3RJSFVLJF9kxkyVjhKqTbHsDQxxjgGHtbR5gwtNgQup8Sj6GvIPGmxGa3MZ18KO_g7zZJTcFO-7NPuTjNuZdnBLg3ECb8ujyBH3y6eHnvUkp2pkAgoV-Y9rYm3Gze5UdOdMmeP24nmbfrz58W31aXH_9-Hl1eb2wpaB8oUTBaF0I1yjq6kYqEKUkFfACiOWsqcsKKimJUIw6cLVhVWklKy1j3KBAdpq9n3n7qUYtFgLKa3U_-M4MOx2N139bgt_odbzTlCiiKiqR4eyRYYg_JkijxthYaFsTAGXrQjHBmKC0Qui7f6C3cRoC6tMYbaZEydn-S8sZtTYtaB_cPuIWewOdt5gK5_H-UhJCOMeBDuezgx1iSgO4w_cp0fsC0FgA-ncBIPbtn3oPyKeMI-BiBmzxld3_mfTqy81M-QtzKr5O</recordid><startdate>202403</startdate><enddate>202403</enddate><creator>Zhang, Chen</creator><creator>Tian, Fafa</creator><creator>Peng, Jing</creator><creator>Wang, Xia</creator><creator>Li, Jingchen</creator><creator>Zhang, Lina</creator><creator>Tan, Zheren</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>IAO</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3758-7824</orcidid></search><sort><creationdate>202403</creationdate><title>Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis‐associated encephalopathy</title><author>Zhang, Chen ; Tian, Fafa ; Peng, Jing ; Wang, Xia ; Li, Jingchen ; Zhang, Lina ; Tan, Zheren</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4715-97231b27fd91fbd89e74806e52e0c53db46e68807931fefba364c834c335a0193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Abdomen</topic><topic>Analysis</topic><topic>Animal cognition</topic><topic>Animal models</topic><topic>Animals</topic><topic>Brain stem</topic><topic>Cecum</topic><topic>Cognition</topic><topic>Cognition disorders</topic><topic>Cognitive ability</topic><topic>cognitive dysfunction</topic><topic>Cognitive Dysfunction - drug therapy</topic><topic>Cognitive Dysfunction - etiology</topic><topic>Cyproheptadine</topic><topic>Cyproheptadine - pharmacology</topic><topic>Cyproheptadine - therapeutic use</topic><topic>Disease Models, Animal</topic><topic>Encephalopathy</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Enzymes</topic><topic>Fluoxetine</topic><topic>Fluoxetine - pharmacology</topic><topic>Fluoxetine - therapeutic use</topic><topic>Frontal lobe</topic><topic>Hippocampus</topic><topic>Humans</topic><topic>Infection</topic><topic>Laboratory animals</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Medical prognosis</topic><topic>Memory</topic><topic>Mice</topic><topic>Motor activity</topic><topic>Neurotransmission</topic><topic>Open-field behavior</topic><topic>Original</topic><topic>Pattern recognition</topic><topic>Sepsis</topic><topic>Sepsis - complications</topic><topic>Sepsis-Associated Encephalopathy - complications</topic><topic>sepsis‐associated encephalopathy</topic><topic>serotonergic neurotransmission</topic><topic>Serotonin</topic><topic>Serotonin S1 receptors</topic><topic>Serotonin S2 receptors</topic><topic>Serotonin uptake inhibitors</topic><topic>therapeutics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Chen</creatorcontrib><creatorcontrib>Tian, Fafa</creatorcontrib><creatorcontrib>Peng, Jing</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Li, Jingchen</creatorcontrib><creatorcontrib>Zhang, Lina</creatorcontrib><creatorcontrib>Tan, Zheren</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</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>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>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Chen</au><au>Tian, Fafa</au><au>Peng, Jing</au><au>Wang, Xia</au><au>Li, Jingchen</au><au>Zhang, Lina</au><au>Tan, Zheren</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis‐associated encephalopathy</atitle><jtitle>CNS neuroscience & therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2024-03</date><risdate>2024</risdate><volume>30</volume><issue>3</issue><spage>e14655</spage><epage>n/a</epage><pages>e14655-n/a</pages><issn>1755-5930</issn><eissn>1755-5949</eissn><abstract>Background
Patients with sepsis‐associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE.
Methods
The mouse models of SAE were established by injection of lipopolysaccharide (LPS, 10 mg/kg, intraperitoneal) and cecal ligation puncture (CLP) respectively. Barnes maze, new object recognition test and open field test were used to evaluate the effects of fluoxetine (selective serotonin reuptake inhibitor) and cyproheptadine (nonselective 5‐HT2 receptor antagonist) on cognition and motor activity of mice. Additionally, WAY100635 (5‐HT1A receptor antagonist) was co‐administered with fluoxetine to explore the mechanism underlying effect of fluoxetine on cognitive impairments of SAE. Enzyme‐linked immunosorbent assay (ELISA) was performed to determine 5‐HT levels in hippocampus, brainstem and frontal lobe of experimental groups.
Results
Both LPS‐induced sepsis and CLP induced sepsis resulted in a notable learning deficit. Fluoxetine ameliorated, while cyproheptadine aggravated, cognitive impairment in two classic mouse models of SAE. The cognition‐enhancing effect of fluoxetine is reversed by WAY100635. Decreased 5‐HT levels in hippocampus, brainstem and frontal lobe were observed in LPS septic model and CLP septic model. Notably, both fluoxetine and cyproheptadine significantly increased 5‐HT levels in those brain regions in LPS septic model. Additionally, fluoxetine significantly increased 5‐HT levels in frontal lobe of CLP septic model.
Conclusions
Our study demonstrated that serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. These findings contribute to identification of novel targets to prevent and arrest cognitive impairment in SAE.
Septic mice exhibited cognitive dysfunction and decreased 5‐HT in brain region associated with cognition, and cognitive performance was mediated by SSRI and 5‐HT receptor antagonist. Serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38433019</pmid><doi>10.1111/cns.14655</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3758-7824</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley-Blackwell Open Access Titles; PubMed Central |
| subjects | Abdomen Analysis Animal cognition Animal models Animals Brain stem Cecum Cognition Cognition disorders Cognitive ability cognitive dysfunction Cognitive Dysfunction - drug therapy Cognitive Dysfunction - etiology Cyproheptadine Cyproheptadine - pharmacology Cyproheptadine - therapeutic use Disease Models, Animal Encephalopathy Enzyme-linked immunosorbent assay Enzymes Fluoxetine Fluoxetine - pharmacology Fluoxetine - therapeutic use Frontal lobe Hippocampus Humans Infection Laboratory animals Lipopolysaccharides Lipopolysaccharides - toxicity Medical prognosis Memory Mice Motor activity Neurotransmission Open-field behavior Original Pattern recognition Sepsis Sepsis - complications Sepsis-Associated Encephalopathy - complications sepsis‐associated encephalopathy serotonergic neurotransmission Serotonin Serotonin S1 receptors Serotonin S2 receptors Serotonin uptake inhibitors therapeutics |
| title | Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis‐associated encephalopathy |
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