Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)
[Display omitted] •Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicit...
Gespeichert in:
| Veröffentlicht in: | Brain research 2022-08, Vol.1789, p.147949-147949, Article 147949 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 147949 |
|---|---|
| container_issue | |
| container_start_page | 147949 |
| container_title | Brain research |
| container_volume | 1789 |
| creator | Narimatsu, Eichi Kakizaki, Ryuichiro Nomura, Kazuhito Sawamoto, Keigo Takahashi, Kazunobu Uemura, Shuji Ishiguro, Masanori |
| description | [Display omitted]
•Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicity.•β1-agonistic action deteriorates glutamate-excitotoxicity.
We investigated the effects of dexmedetomidine, a selective α2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p |
| doi_str_mv | 10.1016/j.brainres.2022.147949 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2671268028</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006899322001731</els_id><sourcerecordid>2671268028</sourcerecordid><originalsourceid>FETCH-LOGICAL-c368t-bda3793a952dd6d7837fea81fb7a61ba32d66f8239ed47faed8cf1c504f52a13</originalsourceid><addsrcrecordid>eNqFkMtOwzAQRS0EoqXwC1WWsHDxI3HsHeWNhEAC9pZjT5CrPIqdVPD3uCqwZTUz0r0zcw9Cc0oWlFBxvlpUwfguQFwwwtiC5qXK1R6aUlkyLFhO9tGUECKwVIpP0FGMqzRyrsghmvCiUFLkZIqaa_hswcHQt975DjLfrkO_gZjBp4UY_QZSNwRjoWnGxoTsvRkH05oBsO_caMFl8asz68HbzME6bD19l51eviwfnl5uXvE1ZhQTonJ6dowOatNEOPmpM_R2e_N2dY8fn-8erpaP2HIhB1w5w0vFjSqYc8KVkpc1GEnrqjSCVoYzJ0QtGVfg8rI24KStqS1IXhfMUD5Dp7u1KcnHCHHQrY_b_00H_Rg1EyVlQhImk1TspDb0MQao9Tr41oQvTYnegtYr_Qtab0HrHehknP_cGKvE78_2SzYJLnYCSEE3HoKO1kOXePkAdtCu9__d-AZBApNc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2671268028</pqid></control><display><type>article</type><title>Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)</title><source>Elsevier ScienceDirect Journals</source><creator>Narimatsu, Eichi ; Kakizaki, Ryuichiro ; Nomura, Kazuhito ; Sawamoto, Keigo ; Takahashi, Kazunobu ; Uemura, Shuji ; Ishiguro, Masanori</creator><creatorcontrib>Narimatsu, Eichi ; Kakizaki, Ryuichiro ; Nomura, Kazuhito ; Sawamoto, Keigo ; Takahashi, Kazunobu ; Uemura, Shuji ; Ishiguro, Masanori</creatorcontrib><description>[Display omitted]
•Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicity.•β1-agonistic action deteriorates glutamate-excitotoxicity.
We investigated the effects of dexmedetomidine, a selective α2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p < 0.05 was accepted as significant. Glutamate (10 mM for 10 min) completely depressed PSs and fEPSPs, which were partially recovered by the following washout for 40 min (57.4 ± 10.2% and 59.9 ± 9.8% of the control, respectively, p < 0.01, n = 6). The recoveries in PSs and fEPSPs were improved by pre-treatment and simultaneous treatment with dexmedetomidine (p < 0.01, n = 6) but were not altered by post-treatment. Dexmedetomidine alone did not alter PSs and fEPSPs. Simultaneous treatment with isoproterenol or dobutamine exacerbated the recoveries in PSs and fEPSPs (p < 0.01, n = 6), but simultaneous treatment with salbutamol, propranolol, phenylephrine or phentramine did not influence the recoveries. Simultaneous treatment with AP5 improved the recoveries in PSs and fEPSPs that were depressed by glutamate alone and by glutamate with dexmedetomidine, isoproterenol or dobutamine (p < 0.01, n = 6). Excessive glutamate depresses glutamatergic excitatory synaptic transmissions by mainly mediating NMDA receptors, and the depressed transmissions are improved by α2-adrenoceptor stimulation but are exacerbated by β1-adrenoceptor stimulation. Dexmedetomidine has a protective effect on neuronal dysfunctions induced by excessive glutamate, which is one of the main mechanisms of the secondary damage in the central nervous system.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2022.147949</identifier><identifier>PMID: 35598640</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Dexmedetomidine ; Excitotoxicity ; Glutamate ; Hippocampus ; NMDA receptor ; Synaptic transmission</subject><ispartof>Brain research, 2022-08, Vol.1789, p.147949-147949, Article 147949</ispartof><rights>2022 Elsevier B.V.</rights><rights>Copyright © 2022 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-bda3793a952dd6d7837fea81fb7a61ba32d66f8239ed47faed8cf1c504f52a13</citedby><cites>FETCH-LOGICAL-c368t-bda3793a952dd6d7837fea81fb7a61ba32d66f8239ed47faed8cf1c504f52a13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006899322001731$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35598640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Narimatsu, Eichi</creatorcontrib><creatorcontrib>Kakizaki, Ryuichiro</creatorcontrib><creatorcontrib>Nomura, Kazuhito</creatorcontrib><creatorcontrib>Sawamoto, Keigo</creatorcontrib><creatorcontrib>Takahashi, Kazunobu</creatorcontrib><creatorcontrib>Uemura, Shuji</creatorcontrib><creatorcontrib>Ishiguro, Masanori</creatorcontrib><title>Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>[Display omitted]
•Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicity.•β1-agonistic action deteriorates glutamate-excitotoxicity.
We investigated the effects of dexmedetomidine, a selective α2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p < 0.05 was accepted as significant. Glutamate (10 mM for 10 min) completely depressed PSs and fEPSPs, which were partially recovered by the following washout for 40 min (57.4 ± 10.2% and 59.9 ± 9.8% of the control, respectively, p < 0.01, n = 6). The recoveries in PSs and fEPSPs were improved by pre-treatment and simultaneous treatment with dexmedetomidine (p < 0.01, n = 6) but were not altered by post-treatment. Dexmedetomidine alone did not alter PSs and fEPSPs. Simultaneous treatment with isoproterenol or dobutamine exacerbated the recoveries in PSs and fEPSPs (p < 0.01, n = 6), but simultaneous treatment with salbutamol, propranolol, phenylephrine or phentramine did not influence the recoveries. Simultaneous treatment with AP5 improved the recoveries in PSs and fEPSPs that were depressed by glutamate alone and by glutamate with dexmedetomidine, isoproterenol or dobutamine (p < 0.01, n = 6). Excessive glutamate depresses glutamatergic excitatory synaptic transmissions by mainly mediating NMDA receptors, and the depressed transmissions are improved by α2-adrenoceptor stimulation but are exacerbated by β1-adrenoceptor stimulation. Dexmedetomidine has a protective effect on neuronal dysfunctions induced by excessive glutamate, which is one of the main mechanisms of the secondary damage in the central nervous system.</description><subject>Dexmedetomidine</subject><subject>Excitotoxicity</subject><subject>Glutamate</subject><subject>Hippocampus</subject><subject>NMDA receptor</subject><subject>Synaptic transmission</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNqFkMtOwzAQRS0EoqXwC1WWsHDxI3HsHeWNhEAC9pZjT5CrPIqdVPD3uCqwZTUz0r0zcw9Cc0oWlFBxvlpUwfguQFwwwtiC5qXK1R6aUlkyLFhO9tGUECKwVIpP0FGMqzRyrsghmvCiUFLkZIqaa_hswcHQt975DjLfrkO_gZjBp4UY_QZSNwRjoWnGxoTsvRkH05oBsO_caMFl8asz68HbzME6bD19l51eviwfnl5uXvE1ZhQTonJ6dowOatNEOPmpM_R2e_N2dY8fn-8erpaP2HIhB1w5w0vFjSqYc8KVkpc1GEnrqjSCVoYzJ0QtGVfg8rI24KStqS1IXhfMUD5Dp7u1KcnHCHHQrY_b_00H_Rg1EyVlQhImk1TspDb0MQao9Tr41oQvTYnegtYr_Qtab0HrHehknP_cGKvE78_2SzYJLnYCSEE3HoKO1kOXePkAdtCu9__d-AZBApNc</recordid><startdate>20220815</startdate><enddate>20220815</enddate><creator>Narimatsu, Eichi</creator><creator>Kakizaki, Ryuichiro</creator><creator>Nomura, Kazuhito</creator><creator>Sawamoto, Keigo</creator><creator>Takahashi, Kazunobu</creator><creator>Uemura, Shuji</creator><creator>Ishiguro, Masanori</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20220815</creationdate><title>Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)</title><author>Narimatsu, Eichi ; Kakizaki, Ryuichiro ; Nomura, Kazuhito ; Sawamoto, Keigo ; Takahashi, Kazunobu ; Uemura, Shuji ; Ishiguro, Masanori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-bda3793a952dd6d7837fea81fb7a61ba32d66f8239ed47faed8cf1c504f52a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Dexmedetomidine</topic><topic>Excitotoxicity</topic><topic>Glutamate</topic><topic>Hippocampus</topic><topic>NMDA receptor</topic><topic>Synaptic transmission</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Narimatsu, Eichi</creatorcontrib><creatorcontrib>Kakizaki, Ryuichiro</creatorcontrib><creatorcontrib>Nomura, Kazuhito</creatorcontrib><creatorcontrib>Sawamoto, Keigo</creatorcontrib><creatorcontrib>Takahashi, Kazunobu</creatorcontrib><creatorcontrib>Uemura, Shuji</creatorcontrib><creatorcontrib>Ishiguro, Masanori</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Narimatsu, Eichi</au><au>Kakizaki, Ryuichiro</au><au>Nomura, Kazuhito</au><au>Sawamoto, Keigo</au><au>Takahashi, Kazunobu</au><au>Uemura, Shuji</au><au>Ishiguro, Masanori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2022-08-15</date><risdate>2022</risdate><volume>1789</volume><spage>147949</spage><epage>147949</epage><pages>147949-147949</pages><artnum>147949</artnum><issn>0006-8993</issn><eissn>1872-6240</eissn><abstract>[Display omitted]
•Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicity.•β1-agonistic action deteriorates glutamate-excitotoxicity.
We investigated the effects of dexmedetomidine, a selective α2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p < 0.05 was accepted as significant. Glutamate (10 mM for 10 min) completely depressed PSs and fEPSPs, which were partially recovered by the following washout for 40 min (57.4 ± 10.2% and 59.9 ± 9.8% of the control, respectively, p < 0.01, n = 6). The recoveries in PSs and fEPSPs were improved by pre-treatment and simultaneous treatment with dexmedetomidine (p < 0.01, n = 6) but were not altered by post-treatment. Dexmedetomidine alone did not alter PSs and fEPSPs. Simultaneous treatment with isoproterenol or dobutamine exacerbated the recoveries in PSs and fEPSPs (p < 0.01, n = 6), but simultaneous treatment with salbutamol, propranolol, phenylephrine or phentramine did not influence the recoveries. Simultaneous treatment with AP5 improved the recoveries in PSs and fEPSPs that were depressed by glutamate alone and by glutamate with dexmedetomidine, isoproterenol or dobutamine (p < 0.01, n = 6). Excessive glutamate depresses glutamatergic excitatory synaptic transmissions by mainly mediating NMDA receptors, and the depressed transmissions are improved by α2-adrenoceptor stimulation but are exacerbated by β1-adrenoceptor stimulation. Dexmedetomidine has a protective effect on neuronal dysfunctions induced by excessive glutamate, which is one of the main mechanisms of the secondary damage in the central nervous system.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>35598640</pmid><doi>10.1016/j.brainres.2022.147949</doi><tpages>1</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-8993 |
| ispartof | Brain research, 2022-08, Vol.1789, p.147949-147949, Article 147949 |
| issn | 0006-8993 1872-6240 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2671268028 |
| source | Elsevier ScienceDirect Journals |
| subjects | Dexmedetomidine Excitotoxicity Glutamate Hippocampus NMDA receptor Synaptic transmission |
| title | Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941) |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T10%3A16%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dexmedetomidine%20improves%20excessive%20extracellular%20glutamate-induced%20synaptic%20depression%20(BRAINRES-D-21-00941)&rft.jtitle=Brain%20research&rft.au=Narimatsu,%20Eichi&rft.date=2022-08-15&rft.volume=1789&rft.spage=147949&rft.epage=147949&rft.pages=147949-147949&rft.artnum=147949&rft.issn=0006-8993&rft.eissn=1872-6240&rft_id=info:doi/10.1016/j.brainres.2022.147949&rft_dat=%3Cproquest_cross%3E2671268028%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2671268028&rft_id=info:pmid/35598640&rft_els_id=S0006899322001731&rfr_iscdi=true |