The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study
Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200 mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either θ-p...
Gespeichert in:
Veröffentlicht in: | Neuropeptides (Edinburgh) 2002-08, Vol.36 (4), p.263-270 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 270 |
---|---|
container_issue | 4 |
container_start_page | 263 |
container_title | Neuropeptides (Edinburgh) |
container_volume | 36 |
creator | Rostampour, M Fathollahi, Y Semnanian, S Hajizadeh, S Mirnajafizadeh, J Shafizadeh, M |
description | Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200
mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either θ-pattern primed bursts (PBs), perfusion with low Mg
2+ or with high Ca
2+, indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed. |
doi_str_mv | 10.1016/S0143-4179(02)00029-X |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72156682</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S014341790200029X</els_id><sourcerecordid>72156682</sourcerecordid><originalsourceid>FETCH-LOGICAL-c443t-ef73a15a0fe584cc1be021191d7271fcbfd943995ea92035c1f7ec702497b0343</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhS1ERYeBRwB5A4JFwH8Zx92gagS0UiUWFKk7y3GuGaMkDrZTlEfhbfH8qF2ysuT7nWPfcxB6RckHSujm43dCBa8EleodYe8JIUxVd0_QitacVUw29VO0ekDO0fOUfhVIsKZ5hs4p45JJQlbo7-0OsGl97_OCg8M7P03BmmEyPd5eUmwiGOxCxH7sZpt9GPdUH8afVYY44ClkGLM3h4lPeIKYfNrf9QuOUDTQ4XbBU_TFJBe3PJQh_uPzDtulkGbwI1xgU-Qjvvc5Bpzy3C0v0JkzfYKXp3ONfnz5fLu9qm6-fb3eXt5UVgieK3CSG1ob4qBuhLW0BcIoVbQrG1JnW9cpwZWqwShGeG2pk2AlYULJlnDB1-jt0XeK4fcMKevBJwt9b0YIc9KS0XqzaVgB6yNoY0gpgtNlqcHERVOi953oQyd6H7gmTB860XdF9_r0wNwO0D2qTiUU4M0JMMma3kUzWp8eObGhXJVe1-jTkYMSx72HqJP1MJaEfQSbdRf8f77yDy__q4A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72156682</pqid></control><display><type>article</type><title>The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Rostampour, M ; Fathollahi, Y ; Semnanian, S ; Hajizadeh, S ; Mirnajafizadeh, J ; Shafizadeh, M</creator><creatorcontrib>Rostampour, M ; Fathollahi, Y ; Semnanian, S ; Hajizadeh, S ; Mirnajafizadeh, J ; Shafizadeh, M</creatorcontrib><description>Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200
mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either θ-pattern primed bursts (PBs), perfusion with low Mg
2+ or with high Ca
2+, indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed.</description><identifier>ISSN: 0143-4179</identifier><identifier>EISSN: 1532-2785</identifier><identifier>DOI: 10.1016/S0143-4179(02)00029-X</identifier><identifier>PMID: 12372700</identifier><identifier>CODEN: NRPPDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Calcium - pharmacology ; Central nervous system ; Cysteamine - pharmacology ; Depression, Chemical ; Electric Stimulation ; Electrophysiology ; Excitatory Postsynaptic Potentials - drug effects ; Fundamental and applied biological sciences. Psychology ; Hippocampus - cytology ; Hippocampus - physiology ; In Vitro Techniques ; Long-Term Potentiation - physiology ; Magnesium - physiology ; Male ; Membrane Potentials - drug effects ; Neurons, Afferent - drug effects ; Pyramidal Cells - drug effects ; Rats ; Synapses - drug effects ; Synaptic Transmission - drug effects ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuropeptides (Edinburgh), 2002-08, Vol.36 (4), p.263-270</ispartof><rights>2002 Elsevier Science Ltd</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2002 Elsevier Science Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-ef73a15a0fe584cc1be021191d7271fcbfd943995ea92035c1f7ec702497b0343</citedby><cites>FETCH-LOGICAL-c443t-ef73a15a0fe584cc1be021191d7271fcbfd943995ea92035c1f7ec702497b0343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S014341790200029X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14613915$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12372700$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rostampour, M</creatorcontrib><creatorcontrib>Fathollahi, Y</creatorcontrib><creatorcontrib>Semnanian, S</creatorcontrib><creatorcontrib>Hajizadeh, S</creatorcontrib><creatorcontrib>Mirnajafizadeh, J</creatorcontrib><creatorcontrib>Shafizadeh, M</creatorcontrib><title>The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study</title><title>Neuropeptides (Edinburgh)</title><addtitle>Neuropeptides</addtitle><description>Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200
mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either θ-pattern primed bursts (PBs), perfusion with low Mg
2+ or with high Ca
2+, indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Central nervous system</subject><subject>Cysteamine - pharmacology</subject><subject>Depression, Chemical</subject><subject>Electric Stimulation</subject><subject>Electrophysiology</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - physiology</subject><subject>In Vitro Techniques</subject><subject>Long-Term Potentiation - physiology</subject><subject>Magnesium - physiology</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>Neurons, Afferent - drug effects</subject><subject>Pyramidal Cells - drug effects</subject><subject>Rats</subject><subject>Synapses - drug effects</subject><subject>Synaptic Transmission - drug effects</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0143-4179</issn><issn>1532-2785</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS1ERYeBRwB5A4JFwH8Zx92gagS0UiUWFKk7y3GuGaMkDrZTlEfhbfH8qF2ysuT7nWPfcxB6RckHSujm43dCBa8EleodYe8JIUxVd0_QitacVUw29VO0ekDO0fOUfhVIsKZ5hs4p45JJQlbo7-0OsGl97_OCg8M7P03BmmEyPd5eUmwiGOxCxH7sZpt9GPdUH8afVYY44ClkGLM3h4lPeIKYfNrf9QuOUDTQ4XbBU_TFJBe3PJQh_uPzDtulkGbwI1xgU-Qjvvc5Bpzy3C0v0JkzfYKXp3ONfnz5fLu9qm6-fb3eXt5UVgieK3CSG1ob4qBuhLW0BcIoVbQrG1JnW9cpwZWqwShGeG2pk2AlYULJlnDB1-jt0XeK4fcMKevBJwt9b0YIc9KS0XqzaVgB6yNoY0gpgtNlqcHERVOi953oQyd6H7gmTB860XdF9_r0wNwO0D2qTiUU4M0JMMma3kUzWp8eObGhXJVe1-jTkYMSx72HqJP1MJaEfQSbdRf8f77yDy__q4A</recordid><startdate>20020801</startdate><enddate>20020801</enddate><creator>Rostampour, M</creator><creator>Fathollahi, Y</creator><creator>Semnanian, S</creator><creator>Hajizadeh, S</creator><creator>Mirnajafizadeh, J</creator><creator>Shafizadeh, M</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20020801</creationdate><title>The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study</title><author>Rostampour, M ; Fathollahi, Y ; Semnanian, S ; Hajizadeh, S ; Mirnajafizadeh, J ; Shafizadeh, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-ef73a15a0fe584cc1be021191d7271fcbfd943995ea92035c1f7ec702497b0343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Central nervous system</topic><topic>Cysteamine - pharmacology</topic><topic>Depression, Chemical</topic><topic>Electric Stimulation</topic><topic>Electrophysiology</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - physiology</topic><topic>In Vitro Techniques</topic><topic>Long-Term Potentiation - physiology</topic><topic>Magnesium - physiology</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>Neurons, Afferent - drug effects</topic><topic>Pyramidal Cells - drug effects</topic><topic>Rats</topic><topic>Synapses - drug effects</topic><topic>Synaptic Transmission - drug effects</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rostampour, M</creatorcontrib><creatorcontrib>Fathollahi, Y</creatorcontrib><creatorcontrib>Semnanian, S</creatorcontrib><creatorcontrib>Hajizadeh, S</creatorcontrib><creatorcontrib>Mirnajafizadeh, J</creatorcontrib><creatorcontrib>Shafizadeh, M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropeptides (Edinburgh)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rostampour, M</au><au>Fathollahi, Y</au><au>Semnanian, S</au><au>Hajizadeh, S</au><au>Mirnajafizadeh, J</au><au>Shafizadeh, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study</atitle><jtitle>Neuropeptides (Edinburgh)</jtitle><addtitle>Neuropeptides</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>36</volume><issue>4</issue><spage>263</spage><epage>270</epage><pages>263-270</pages><issn>0143-4179</issn><eissn>1532-2785</eissn><coden>NRPPDD</coden><abstract>Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200
mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either θ-pattern primed bursts (PBs), perfusion with low Mg
2+ or with high Ca
2+, indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12372700</pmid><doi>10.1016/S0143-4179(02)00029-X</doi><tpages>8</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0143-4179 |
ispartof | Neuropeptides (Edinburgh), 2002-08, Vol.36 (4), p.263-270 |
issn | 0143-4179 1532-2785 |
language | eng |
recordid | cdi_proquest_miscellaneous_72156682 |
source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | Animals Biological and medical sciences Calcium - pharmacology Central nervous system Cysteamine - pharmacology Depression, Chemical Electric Stimulation Electrophysiology Excitatory Postsynaptic Potentials - drug effects Fundamental and applied biological sciences. Psychology Hippocampus - cytology Hippocampus - physiology In Vitro Techniques Long-Term Potentiation - physiology Magnesium - physiology Male Membrane Potentials - drug effects Neurons, Afferent - drug effects Pyramidal Cells - drug effects Rats Synapses - drug effects Synaptic Transmission - drug effects Vertebrates: nervous system and sense organs |
title | The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T05%3A49%3A15IST&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=The%20ability%20of%20hippocampal%20CA1%20area%20for%20induction%20of%20long-term%20potentiation%20is%20persistently%20reduced%20by%20prior%20treatment%20with%20cysteamine:%20an%20in%20vitro%20study&rft.jtitle=Neuropeptides%20(Edinburgh)&rft.au=Rostampour,%20M&rft.date=2002-08-01&rft.volume=36&rft.issue=4&rft.spage=263&rft.epage=270&rft.pages=263-270&rft.issn=0143-4179&rft.eissn=1532-2785&rft.coden=NRPPDD&rft_id=info:doi/10.1016/S0143-4179(02)00029-X&rft_dat=%3Cproquest_cross%3E72156682%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=72156682&rft_id=info:pmid/12372700&rft_els_id=S014341790200029X&rfr_iscdi=true |