SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, selectively inhibits N‐type calcium currents in cultured hippocampal neurons
1 Whole‐cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, on voltage‐sensitive channels. 2 SO‐3 had no effect on voltage‐sensitive sodium currents, delayed rectifier potassium currents, and tra...
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| Veröffentlicht in: | British journal of pharmacology 2005-07, Vol.145 (6), p.728-739 |
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| creator | Wen, Lei Yang, Sheng Qiao, Haifa Liu, Zhenwei Zhou, Wenxia Zhang, Yongxiang Huang, Peitang |
| description | 1
Whole‐cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, on voltage‐sensitive channels.
2
SO‐3 had no effect on voltage‐sensitive sodium currents, delayed rectifier potassium currents, and transient outward potassium currents.
3
Similar to the selective N‐type calcium channel blocker ω‐conotoxin MVIIA (MVIIA), SO‐3 could concentration‐dependently inhibit the high voltage‐activated (HVA) calcium currents (ICa).
4
MVIIA(3 μM), 10 μM nimodipine, and 0.5 μM ω‐agatoxin IVA (Aga) could selectively block the N‐, L‐, and P/Q‐type ICa, which contributed ∼32, ∼38, and ∼21% of the HVA currents in hippocampal neurons, respectively. About 31% of the total HVA currents were inhibited by 3 μM SO‐3. SO‐3 (3 μM) and 3 μM MVIIA inhibited the overlapping components of HVA currents, whereas no overlapping component was inhibited by 3 μM SO‐3 and 10 μM nimodipine, or by 3 μM SO‐3 and 0.5 μM Aga. Also, 3 μM SO‐3 had no effect on R‐type currents.
5
SO‐3 had less inhibitory effects on non‐N‐type HVA currents than MVIIA at higher concentrations (30 and 100 μM).
6
The inhibitory effects of SO‐3 and MVIIA on HVA currents were almost fully reversible. However, the recovery from block by MVIIA was more rapid than recovery from block by SO‐3.
7
It is concluded that SO‐3 is a new ω‐conotoxin selectively targeting N‐type voltage‐sensitive calcium channels. Considering the significance of N‐type calcium channels for pain transduction, SO‐3 may have therapeutic potential as a novel analgesic agent.
British Journal of Pharmacology (2005) 145, 728–739. doi:10.1038/sj.bjp.0706223 |
| doi_str_mv | 10.1038/sj.bjp.0706223 |
| format | Article |
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Whole‐cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, on voltage‐sensitive channels.
2
SO‐3 had no effect on voltage‐sensitive sodium currents, delayed rectifier potassium currents, and transient outward potassium currents.
3
Similar to the selective N‐type calcium channel blocker ω‐conotoxin MVIIA (MVIIA), SO‐3 could concentration‐dependently inhibit the high voltage‐activated (HVA) calcium currents (ICa).
4
MVIIA(3 μM), 10 μM nimodipine, and 0.5 μM ω‐agatoxin IVA (Aga) could selectively block the N‐, L‐, and P/Q‐type ICa, which contributed ∼32, ∼38, and ∼21% of the HVA currents in hippocampal neurons, respectively. About 31% of the total HVA currents were inhibited by 3 μM SO‐3. SO‐3 (3 μM) and 3 μM MVIIA inhibited the overlapping components of HVA currents, whereas no overlapping component was inhibited by 3 μM SO‐3 and 10 μM nimodipine, or by 3 μM SO‐3 and 0.5 μM Aga. Also, 3 μM SO‐3 had no effect on R‐type currents.
5
SO‐3 had less inhibitory effects on non‐N‐type HVA currents than MVIIA at higher concentrations (30 and 100 μM).
6
The inhibitory effects of SO‐3 and MVIIA on HVA currents were almost fully reversible. However, the recovery from block by MVIIA was more rapid than recovery from block by SO‐3.
7
It is concluded that SO‐3 is a new ω‐conotoxin selectively targeting N‐type voltage‐sensitive calcium channels. Considering the significance of N‐type calcium channels for pain transduction, SO‐3 may have therapeutic potential as a novel analgesic agent.
British Journal of Pharmacology (2005) 145, 728–739. doi:10.1038/sj.bjp.0706223</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706223</identifier><identifier>PMID: 15880145</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Amino Acid Sequence ; Animals ; Biological and medical sciences ; Calcium Channel Blockers - pharmacology ; Calcium Channels, N-Type - drug effects ; Calcium Channels, N-Type - physiology ; Cells, Cultured ; Conus striatus ; hippocampal neurons ; Hippocampus - drug effects ; Hippocampus - physiology ; Marine ; Medical sciences ; Membrane Potentials - drug effects ; Molecular Sequence Data ; Neurons - drug effects ; Neurons - physiology ; Nimodipine - pharmacology ; N‐type calcium channel blockers ; omega-Agatoxin IVA - pharmacology ; omega-Conotoxins - pharmacology ; pain ; Patch-Clamp Techniques ; Peptides - pharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; SO‐3 ; voltage‐sensitive calcium channels ; voltage‐sensitive potassium channels ; voltage‐sensitive sodium channels ; ω‐conotoxins</subject><ispartof>British journal of pharmacology, 2005-07, Vol.145 (6), p.728-739</ispartof><rights>2005 British Pharmacological Society</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2005</rights><rights>Copyright 2005, Nature Publishing Group 2005 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5205-8b49791bc47cf36185fba99e3892ab411ba50f2dc7d7c3b54b2f9f19e9c0b753</citedby><cites>FETCH-LOGICAL-c5205-8b49791bc47cf36185fba99e3892ab411ba50f2dc7d7c3b54b2f9f19e9c0b753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576188/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576188/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16955855$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15880145$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wen, Lei</creatorcontrib><creatorcontrib>Yang, Sheng</creatorcontrib><creatorcontrib>Qiao, Haifa</creatorcontrib><creatorcontrib>Liu, Zhenwei</creatorcontrib><creatorcontrib>Zhou, Wenxia</creatorcontrib><creatorcontrib>Zhang, Yongxiang</creatorcontrib><creatorcontrib>Huang, Peitang</creatorcontrib><title>SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, selectively inhibits N‐type calcium currents in cultured hippocampal neurons</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
Whole‐cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, on voltage‐sensitive channels.
2
SO‐3 had no effect on voltage‐sensitive sodium currents, delayed rectifier potassium currents, and transient outward potassium currents.
3
Similar to the selective N‐type calcium channel blocker ω‐conotoxin MVIIA (MVIIA), SO‐3 could concentration‐dependently inhibit the high voltage‐activated (HVA) calcium currents (ICa).
4
MVIIA(3 μM), 10 μM nimodipine, and 0.5 μM ω‐agatoxin IVA (Aga) could selectively block the N‐, L‐, and P/Q‐type ICa, which contributed ∼32, ∼38, and ∼21% of the HVA currents in hippocampal neurons, respectively. About 31% of the total HVA currents were inhibited by 3 μM SO‐3. SO‐3 (3 μM) and 3 μM MVIIA inhibited the overlapping components of HVA currents, whereas no overlapping component was inhibited by 3 μM SO‐3 and 10 μM nimodipine, or by 3 μM SO‐3 and 0.5 μM Aga. Also, 3 μM SO‐3 had no effect on R‐type currents.
5
SO‐3 had less inhibitory effects on non‐N‐type HVA currents than MVIIA at higher concentrations (30 and 100 μM).
6
The inhibitory effects of SO‐3 and MVIIA on HVA currents were almost fully reversible. However, the recovery from block by MVIIA was more rapid than recovery from block by SO‐3.
7
It is concluded that SO‐3 is a new ω‐conotoxin selectively targeting N‐type voltage‐sensitive calcium channels. Considering the significance of N‐type calcium channels for pain transduction, SO‐3 may have therapeutic potential as a novel analgesic agent.
British Journal of Pharmacology (2005) 145, 728–739. doi:10.1038/sj.bjp.0706223</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels, N-Type - drug effects</subject><subject>Calcium Channels, N-Type - physiology</subject><subject>Cells, Cultured</subject><subject>Conus striatus</subject><subject>hippocampal neurons</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiology</subject><subject>Marine</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Molecular Sequence Data</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Nimodipine - pharmacology</subject><subject>N‐type calcium channel blockers</subject><subject>omega-Agatoxin IVA - pharmacology</subject><subject>omega-Conotoxins - pharmacology</subject><subject>pain</subject><subject>Patch-Clamp Techniques</subject><subject>Peptides - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>SO‐3</subject><subject>voltage‐sensitive calcium channels</subject><subject>voltage‐sensitive potassium channels</subject><subject>voltage‐sensitive sodium channels</subject><subject>ω‐conotoxins</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><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>eNqFkcGOFCEURStG47SjW5eGmOhqqoWiKKjNJNpRx2TimDh7AhTYdCgooZhJ7_wEN_6gXyKdrjjqxg3w8s6775JbVU8RXCOI2au0W8vdtIYUdk2D71Ur1NKuJpih-9UKQkhrhBg7qR6ltIOwNCl5WJ0gwlgpyKr68fnq57fv-AwI4PUtOBQpTzoaMVq3Byr4MOlptoMGg472Rg_AxDCCTfA5gTRHK-aczkDSTqu59MuQ9Vsr7ZzAx6I27ycNlHDK5hGoHKP2pWN9ebs5x6K3tdMUlBgn4YqHHINPj6sHRriknyz3aXX97u315qK-vHr_YfP6slakgaRmsu1pj6RqqTK4Q4wYKfpeY9Y3QrYISUGgaQZFB6qwJK1sTG9Qr3sFJSX4tDo_yk5ZjnpQxVoUjk_RjiLueRCW_93xdsu_hBuOCC3bWBF4uQjE8DXrNPPRJqWdE16HnDiiuOtQ1xbw-T_gLuToy994g2gDYTkLtD5CKoaUoja_nSDID2nztOMlbb6kXQae_en_Dl_iLcCLBRCpZGCi8MqmO67rCWHkwOEjd2ud3v9nLX_z6aLpIcG_AJtZypg</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Wen, Lei</creator><creator>Yang, Sheng</creator><creator>Qiao, Haifa</creator><creator>Liu, Zhenwei</creator><creator>Zhou, Wenxia</creator><creator>Zhang, Yongxiang</creator><creator>Huang, Peitang</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>F1W</scope><scope>H95</scope><scope>L.G</scope><scope>5PM</scope></search><sort><creationdate>200507</creationdate><title>SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, selectively inhibits N‐type calcium currents in cultured hippocampal neurons</title><author>Wen, Lei ; Yang, Sheng ; Qiao, Haifa ; Liu, Zhenwei ; Zhou, Wenxia ; Zhang, Yongxiang ; Huang, Peitang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5205-8b49791bc47cf36185fba99e3892ab411ba50f2dc7d7c3b54b2f9f19e9c0b753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels, N-Type - drug effects</topic><topic>Calcium Channels, N-Type - physiology</topic><topic>Cells, Cultured</topic><topic>Conus striatus</topic><topic>hippocampal neurons</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiology</topic><topic>Marine</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Molecular Sequence Data</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Nimodipine - pharmacology</topic><topic>N‐type calcium channel blockers</topic><topic>omega-Agatoxin IVA - pharmacology</topic><topic>omega-Conotoxins - pharmacology</topic><topic>pain</topic><topic>Patch-Clamp Techniques</topic><topic>Peptides - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>SO‐3</topic><topic>voltage‐sensitive calcium channels</topic><topic>voltage‐sensitive potassium channels</topic><topic>voltage‐sensitive sodium channels</topic><topic>ω‐conotoxins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wen, Lei</creatorcontrib><creatorcontrib>Yang, Sheng</creatorcontrib><creatorcontrib>Qiao, Haifa</creatorcontrib><creatorcontrib>Liu, Zhenwei</creatorcontrib><creatorcontrib>Zhou, Wenxia</creatorcontrib><creatorcontrib>Zhang, Yongxiang</creatorcontrib><creatorcontrib>Huang, Peitang</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wen, Lei</au><au>Yang, Sheng</au><au>Qiao, Haifa</au><au>Liu, Zhenwei</au><au>Zhou, Wenxia</au><au>Zhang, Yongxiang</au><au>Huang, Peitang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, selectively inhibits N‐type calcium currents in cultured hippocampal neurons</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2005-07</date><risdate>2005</risdate><volume>145</volume><issue>6</issue><spage>728</spage><epage>739</epage><pages>728-739</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
Whole‐cell currents in cultured hippocampal neurons were recorded to investigate the effects of SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, on voltage‐sensitive channels.
2
SO‐3 had no effect on voltage‐sensitive sodium currents, delayed rectifier potassium currents, and transient outward potassium currents.
3
Similar to the selective N‐type calcium channel blocker ω‐conotoxin MVIIA (MVIIA), SO‐3 could concentration‐dependently inhibit the high voltage‐activated (HVA) calcium currents (ICa).
4
MVIIA(3 μM), 10 μM nimodipine, and 0.5 μM ω‐agatoxin IVA (Aga) could selectively block the N‐, L‐, and P/Q‐type ICa, which contributed ∼32, ∼38, and ∼21% of the HVA currents in hippocampal neurons, respectively. About 31% of the total HVA currents were inhibited by 3 μM SO‐3. SO‐3 (3 μM) and 3 μM MVIIA inhibited the overlapping components of HVA currents, whereas no overlapping component was inhibited by 3 μM SO‐3 and 10 μM nimodipine, or by 3 μM SO‐3 and 0.5 μM Aga. Also, 3 μM SO‐3 had no effect on R‐type currents.
5
SO‐3 had less inhibitory effects on non‐N‐type HVA currents than MVIIA at higher concentrations (30 and 100 μM).
6
The inhibitory effects of SO‐3 and MVIIA on HVA currents were almost fully reversible. However, the recovery from block by MVIIA was more rapid than recovery from block by SO‐3.
7
It is concluded that SO‐3 is a new ω‐conotoxin selectively targeting N‐type voltage‐sensitive calcium channels. Considering the significance of N‐type calcium channels for pain transduction, SO‐3 may have therapeutic potential as a novel analgesic agent.
British Journal of Pharmacology (2005) 145, 728–739. doi:10.1038/sj.bjp.0706223</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15880145</pmid><doi>10.1038/sj.bjp.0706223</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acid Sequence Animals Biological and medical sciences Calcium Channel Blockers - pharmacology Calcium Channels, N-Type - drug effects Calcium Channels, N-Type - physiology Cells, Cultured Conus striatus hippocampal neurons Hippocampus - drug effects Hippocampus - physiology Marine Medical sciences Membrane Potentials - drug effects Molecular Sequence Data Neurons - drug effects Neurons - physiology Nimodipine - pharmacology N‐type calcium channel blockers omega-Agatoxin IVA - pharmacology omega-Conotoxins - pharmacology pain Patch-Clamp Techniques Peptides - pharmacology Pharmacology. Drug treatments Rats Rats, Wistar SO‐3 voltage‐sensitive calcium channels voltage‐sensitive potassium channels voltage‐sensitive sodium channels ω‐conotoxins |
| title | SO‐3, a new O‐superfamily conopeptide derived from Conus striatus, selectively inhibits N‐type calcium currents in cultured hippocampal neurons |
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