Postischemic alterations of spontaneous activities in rat hippocampal CA1 neurons
Changes of spontaneous impulse discharges in rat hippocampal neurons during and after transient forebrain ischemia were investigated electrophysiologically. Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was5.8 ± 1.2 (means±S.E....
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| Veröffentlicht in: | Brain research 1990-10, Vol.530 (2), p.257-260 |
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| creator | Furukawa, Katsutoshi Yamana, Kenjirou Kogure, Kyuya |
| description | Changes of spontaneous impulse discharges in rat hippocampal neurons during and after transient forebrain ischemia were investigated electrophysiologically. Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was5.8 ± 1.2 (means±S.E., n = 36). These spontaneous discharges were completely suppressed during forebrain ischemia exept for the transient hyperactivity observed just after the beginning of ischemia. Recovery of spontaneous discharges of CA1 neurons from suppression induced by 5 min ischemia started at 5 min, and neuronal activities were restored to pre-ischemic levels approximately 30 min after reperfusion. On the other hand, spontaneous impulse frequencies at all time points recorded after 20 min ischemia were less than 40% of the pre-ischemic levels. These continuous suppression of spontaneous activity after 20 min ischemia may suggest that neuronal function is impaired during and/or in the early stages of reperfusion, and functional disorders precede morphological degeneration. |
| doi_str_mv | 10.1016/0006-8993(90)91292-O |
| format | Article |
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Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was5.8 ± 1.2 (means±S.E., n = 36). These spontaneous discharges were completely suppressed during forebrain ischemia exept for the transient hyperactivity observed just after the beginning of ischemia. Recovery of spontaneous discharges of CA1 neurons from suppression induced by 5 min ischemia started at 5 min, and neuronal activities were restored to pre-ischemic levels approximately 30 min after reperfusion. On the other hand, spontaneous impulse frequencies at all time points recorded after 20 min ischemia were less than 40% of the pre-ischemic levels. These continuous suppression of spontaneous activity after 20 min ischemia may suggest that neuronal function is impaired during and/or in the early stages of reperfusion, and functional disorders precede morphological degeneration.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0006-8993(90)91292-O</identifier><identifier>PMID: 2265357</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Anesthesia ; Animals ; Delayed neuronal death ; Electrophysiology ; Hippocampus ; Hippocampus - cytology ; Hippocampus - physiopathology ; Ischemia ; Ischemic Attack, Transient - physiopathology ; Male ; Neuronal activity ; Neurons - physiology ; Rat ; Rats ; Rats, Inbred Strains ; Reperfusion</subject><ispartof>Brain research, 1990-10, Vol.530 (2), p.257-260</ispartof><rights>1990 Elsevier Science Publishers B.V. 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Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was5.8 ± 1.2 (means±S.E., n = 36). These spontaneous discharges were completely suppressed during forebrain ischemia exept for the transient hyperactivity observed just after the beginning of ischemia. Recovery of spontaneous discharges of CA1 neurons from suppression induced by 5 min ischemia started at 5 min, and neuronal activities were restored to pre-ischemic levels approximately 30 min after reperfusion. On the other hand, spontaneous impulse frequencies at all time points recorded after 20 min ischemia were less than 40% of the pre-ischemic levels. These continuous suppression of spontaneous activity after 20 min ischemia may suggest that neuronal function is impaired during and/or in the early stages of reperfusion, and functional disorders precede morphological degeneration.</description><subject>Anesthesia</subject><subject>Animals</subject><subject>Delayed neuronal death</subject><subject>Electrophysiology</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - physiopathology</subject><subject>Ischemia</subject><subject>Ischemic Attack, Transient - physiopathology</subject><subject>Male</subject><subject>Neuronal activity</subject><subject>Neurons - physiology</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Reperfusion</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1q3DAUhUVoSCc_b5CCVqVdONGPLUubwjC0aSAwKTRrIctXRMW2XEkeyNtHkxmybFdC3O8cXX0IXVNyQwkVt4QQUUml-BdFvirKFKu2J2hFZcsqwWryAa3ekY_oPKU_5cq5ImfojDHR8KZdoV-PIWWf7DOM3mIzZIgm-zAlHBxOc5iymSAsCRub_c5nDwn7CRcIP_t5DtaMsxnwZk3xBEsswUt06syQ4Op4XqCnH99_b35WD9u7-836obJcylwpZ2vX1aQTINqasQaEcw30QFplXMNYzySXQJ1xPdS1ouCEbKDjjrvauY5foM-H3jmGvwukrMfyDxiGw8JaEqo4bcV_QdpIUvqbAtYH0MaQUgSn5-hHE180JXqvXO996r1PrYh-U663Jfbp2L90I_TvoaPjMv92mEOxsfMQdbIeJgu9j2Cz7oP_9wOv4KOR8w</recordid><startdate>19901022</startdate><enddate>19901022</enddate><creator>Furukawa, Katsutoshi</creator><creator>Yamana, Kenjirou</creator><creator>Kogure, Kyuya</creator><general>Elsevier 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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19901022</creationdate><title>Postischemic alterations of spontaneous activities in rat hippocampal CA1 neurons</title><author>Furukawa, Katsutoshi ; Yamana, Kenjirou ; Kogure, Kyuya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-9fc4fb40b6e674225e6ff5ede079af522d2838e1fafde4491ef685eb3f3f4ffb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Anesthesia</topic><topic>Animals</topic><topic>Delayed neuronal death</topic><topic>Electrophysiology</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - physiopathology</topic><topic>Ischemia</topic><topic>Ischemic Attack, Transient - physiopathology</topic><topic>Male</topic><topic>Neuronal activity</topic><topic>Neurons - physiology</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Reperfusion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Furukawa, Katsutoshi</creatorcontrib><creatorcontrib>Yamana, Kenjirou</creatorcontrib><creatorcontrib>Kogure, Kyuya</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Furukawa, Katsutoshi</au><au>Yamana, Kenjirou</au><au>Kogure, Kyuya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Postischemic alterations of spontaneous activities in rat hippocampal CA1 neurons</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1990-10-22</date><risdate>1990</risdate><volume>530</volume><issue>2</issue><spage>257</spage><epage>260</epage><pages>257-260</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><abstract>Changes of spontaneous impulse discharges in rat hippocampal neurons during and after transient forebrain ischemia were investigated electrophysiologically. Spontaneous impulse frequencies of CA1 neurons before ischemia were varied from 0.4 to 20.0 impulses/s and its average was5.8 ± 1.2 (means±S.E., n = 36). These spontaneous discharges were completely suppressed during forebrain ischemia exept for the transient hyperactivity observed just after the beginning of ischemia. Recovery of spontaneous discharges of CA1 neurons from suppression induced by 5 min ischemia started at 5 min, and neuronal activities were restored to pre-ischemic levels approximately 30 min after reperfusion. On the other hand, spontaneous impulse frequencies at all time points recorded after 20 min ischemia were less than 40% of the pre-ischemic levels. These continuous suppression of spontaneous activity after 20 min ischemia may suggest that neuronal function is impaired during and/or in the early stages of reperfusion, and functional disorders precede morphological degeneration.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>2265357</pmid><doi>10.1016/0006-8993(90)91292-O</doi><tpages>4</tpages></addata></record> |
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| ispartof | Brain research, 1990-10, Vol.530 (2), p.257-260 |
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| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Anesthesia Animals Delayed neuronal death Electrophysiology Hippocampus Hippocampus - cytology Hippocampus - physiopathology Ischemia Ischemic Attack, Transient - physiopathology Male Neuronal activity Neurons - physiology Rat Rats Rats, Inbred Strains Reperfusion |
| title | Postischemic alterations of spontaneous activities in rat hippocampal CA1 neurons |
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