An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system
Reversible blockade of sodium channels by endogenous substances has been claimed to account for the fast exacerbations and relapses commonly seen in demyelinating autoimmune diseases 2 , 3 , 4 . Evidence has been provided that in the cerebrospinal fluid of patients with multiple sclerosis 5 or Guill...
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| Veröffentlicht in: | Nature medicine 2000-07, Vol.6 (7), p.808-811 |
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| creator | Brinkmeier, Heinrich Aulkemeyer, Peter Wollinsky, Kurt H. Rüdel, Reinhardt |
| description | Reversible blockade of sodium channels by endogenous substances has been claimed to account for the fast exacerbations and relapses commonly seen in demyelinating autoimmune diseases
2
,
3
,
4
. Evidence has been provided that in the cerebrospinal fluid of patients with multiple sclerosis
5
or Guillain-Barré syndrome
6
, a sodium-channel-blocking factor exists that has properties of local anesthetic agents
7
,
8
. This factor could contribute to the nerve conduction block and paresis seen in these disorders
9
,
10
,
11
. We describe here a previously unknown endogenous substance in human cerebrospinal fluid with distinct channel-blocking properties even at very low (0.00001 M) concentrations. The pentapeptide with the sequence Gln-Tyr-Asn-Ala-Asp exerted its blocking action by shifting the steady-state inactivation curve of the sodium channels to more-negative potentials, as most local anesthetics do. In the cerebrospinal fluid of healthy individuals, its concentration was about 3 μM, whereas in patients with multiple sclerosis and Guillain-Barré syndrome, it increased 300–1,400%. At these concentrations, the peptide's blocking efficacy was higher than that of 50 μM lidocaine. At a concentration of 10 μM, lidocaine is able to ‘unmask’ subclinical lesions in multiple sclerosis
12
; thus, the endogenous pentapeptide may well contribute to the fast changes of symptoms. Furthermore, it may become valuable as a marker of disease activity. |
| doi_str_mv | 10.1038/77543 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_71219685</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A194204135</galeid><sourcerecordid>A194204135</sourcerecordid><originalsourceid>FETCH-LOGICAL-c538t-a0a49dee16abb03dace6f3e9cf6532f63bd7d1c6c70626b0f832efad70986fc23</originalsourceid><addsrcrecordid>eNqNkt1r1TAYxosobs79CxIEB150Jk2btpeHselgMPAL70qavOnJzEdNUvHc7U83xzPYjgyUBBKS3_u8ycNTFMcEnxJMu3dt29T0SXFImpqVpMXfnuY9bruy6xt2ULyI8QZjTHHTPy8OCO66rqfksLhdOQRO-gmcXyKawSU-w5y0BMRF0m5CPCKOopd6sUisuXNg0Gi8-A4BaZenMtxannzYIL4kr61dHCCpow8SQkReobQGJLJ24AY5CD-3veImJrAvi2eKmwjHd-tR8eXi_PPZh_Lq-v3l2eqqFA3tUskxr3sJQBgfR0wlF8AUhV4o1tBKMTrKVhLBRItZxUasOlqB4rLFfceUqOhRcbLTnYP_sUBMg9VRgDHcQX7N0JKK9Kxr_gmSlrGmp3UGX_8F3vgluPyJoapolqN1n6FyB03cwJC98tkDkd2GbIV3oHQ-XpG-rnBN6Lb76SN8HhKsFo8WvN0ryEyCX2niS4zD5aeP_89ef91nTx6wa-AmraM3S9LexX3wzQ4UwccYQA1z0JaHzUDwsI3m8CeamXt1Z9cyWpAPqF0W7zvGfOUmCPd-7iv9BnNE6QE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>223121349</pqid></control><display><type>article</type><title>An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system</title><source>MEDLINE</source><source>Nature</source><source>SpringerLink Journals - AutoHoldings</source><creator>Brinkmeier, Heinrich ; Aulkemeyer, Peter ; Wollinsky, Kurt H. ; Rüdel, Reinhardt</creator><creatorcontrib>Brinkmeier, Heinrich ; Aulkemeyer, Peter ; Wollinsky, Kurt H. ; Rüdel, Reinhardt</creatorcontrib><description>Reversible blockade of sodium channels by endogenous substances has been claimed to account for the fast exacerbations and relapses commonly seen in demyelinating autoimmune diseases
2
,
3
,
4
. Evidence has been provided that in the cerebrospinal fluid of patients with multiple sclerosis
5
or Guillain-Barré syndrome
6
, a sodium-channel-blocking factor exists that has properties of local anesthetic agents
7
,
8
. This factor could contribute to the nerve conduction block and paresis seen in these disorders
9
,
10
,
11
. We describe here a previously unknown endogenous substance in human cerebrospinal fluid with distinct channel-blocking properties even at very low (0.00001 M) concentrations. The pentapeptide with the sequence Gln-Tyr-Asn-Ala-Asp exerted its blocking action by shifting the steady-state inactivation curve of the sodium channels to more-negative potentials, as most local anesthetics do. In the cerebrospinal fluid of healthy individuals, its concentration was about 3 μM, whereas in patients with multiple sclerosis and Guillain-Barré syndrome, it increased 300–1,400%. At these concentrations, the peptide's blocking efficacy was higher than that of 50 μM lidocaine. At a concentration of 10 μM, lidocaine is able to ‘unmask’ subclinical lesions in multiple sclerosis
12
; thus, the endogenous pentapeptide may well contribute to the fast changes of symptoms. Furthermore, it may become valuable as a marker of disease activity.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/77543</identifier><identifier>PMID: 10888931</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Central nervous system ; Cerebrospinal fluid ; Cerebrospinal Fluid - chemistry ; Chromatography ; Guillain-Barre Syndrome - cerebrospinal fluid ; Humans ; Inactivation ; Infectious Diseases ; Lesions ; Metabolic Diseases ; Molecular Medicine ; Molecular weight ; Multiple sclerosis ; Multiple Sclerosis - cerebrospinal fluid ; Neurons - drug effects ; Neurosciences ; Oligopeptides - isolation & purification ; Oligopeptides - pharmacology ; Patients ; pentapeptides ; Peptides ; Sequence Analysis, Protein ; Sodium ; sodium antagonists ; Sodium Channel Blockers ; Tumor Cells, Cultured</subject><ispartof>Nature medicine, 2000-07, Vol.6 (7), p.808-811</ispartof><rights>Nature America Inc. 2000</rights><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-a0a49dee16abb03dace6f3e9cf6532f63bd7d1c6c70626b0f832efad70986fc23</citedby><cites>FETCH-LOGICAL-c538t-a0a49dee16abb03dace6f3e9cf6532f63bd7d1c6c70626b0f832efad70986fc23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/77543$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/77543$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10888931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brinkmeier, Heinrich</creatorcontrib><creatorcontrib>Aulkemeyer, Peter</creatorcontrib><creatorcontrib>Wollinsky, Kurt H.</creatorcontrib><creatorcontrib>Rüdel, Reinhardt</creatorcontrib><title>An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>Reversible blockade of sodium channels by endogenous substances has been claimed to account for the fast exacerbations and relapses commonly seen in demyelinating autoimmune diseases
2
,
3
,
4
. Evidence has been provided that in the cerebrospinal fluid of patients with multiple sclerosis
5
or Guillain-Barré syndrome
6
, a sodium-channel-blocking factor exists that has properties of local anesthetic agents
7
,
8
. This factor could contribute to the nerve conduction block and paresis seen in these disorders
9
,
10
,
11
. We describe here a previously unknown endogenous substance in human cerebrospinal fluid with distinct channel-blocking properties even at very low (0.00001 M) concentrations. The pentapeptide with the sequence Gln-Tyr-Asn-Ala-Asp exerted its blocking action by shifting the steady-state inactivation curve of the sodium channels to more-negative potentials, as most local anesthetics do. In the cerebrospinal fluid of healthy individuals, its concentration was about 3 μM, whereas in patients with multiple sclerosis and Guillain-Barré syndrome, it increased 300–1,400%. At these concentrations, the peptide's blocking efficacy was higher than that of 50 μM lidocaine. At a concentration of 10 μM, lidocaine is able to ‘unmask’ subclinical lesions in multiple sclerosis
12
; thus, the endogenous pentapeptide may well contribute to the fast changes of symptoms. Furthermore, it may become valuable as a marker of disease activity.</description><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Central nervous system</subject><subject>Cerebrospinal fluid</subject><subject>Cerebrospinal Fluid - chemistry</subject><subject>Chromatography</subject><subject>Guillain-Barre Syndrome - cerebrospinal fluid</subject><subject>Humans</subject><subject>Inactivation</subject><subject>Infectious Diseases</subject><subject>Lesions</subject><subject>Metabolic Diseases</subject><subject>Molecular Medicine</subject><subject>Molecular weight</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - cerebrospinal fluid</subject><subject>Neurons - drug effects</subject><subject>Neurosciences</subject><subject>Oligopeptides - isolation & purification</subject><subject>Oligopeptides - pharmacology</subject><subject>Patients</subject><subject>pentapeptides</subject><subject>Peptides</subject><subject>Sequence Analysis, Protein</subject><subject>Sodium</subject><subject>sodium antagonists</subject><subject>Sodium Channel Blockers</subject><subject>Tumor Cells, Cultured</subject><issn>1078-8956</issn><issn>1546-170X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkt1r1TAYxosobs79CxIEB150Jk2btpeHselgMPAL70qavOnJzEdNUvHc7U83xzPYjgyUBBKS3_u8ycNTFMcEnxJMu3dt29T0SXFImpqVpMXfnuY9bruy6xt2ULyI8QZjTHHTPy8OCO66rqfksLhdOQRO-gmcXyKawSU-w5y0BMRF0m5CPCKOopd6sUisuXNg0Gi8-A4BaZenMtxannzYIL4kr61dHCCpow8SQkReobQGJLJ24AY5CD-3veImJrAvi2eKmwjHd-tR8eXi_PPZh_Lq-v3l2eqqFA3tUskxr3sJQBgfR0wlF8AUhV4o1tBKMTrKVhLBRItZxUasOlqB4rLFfceUqOhRcbLTnYP_sUBMg9VRgDHcQX7N0JKK9Kxr_gmSlrGmp3UGX_8F3vgluPyJoapolqN1n6FyB03cwJC98tkDkd2GbIV3oHQ-XpG-rnBN6Lb76SN8HhKsFo8WvN0ryEyCX2niS4zD5aeP_89ef91nTx6wa-AmraM3S9LexX3wzQ4UwccYQA1z0JaHzUDwsI3m8CeamXt1Z9cyWpAPqF0W7zvGfOUmCPd-7iv9BnNE6QE</recordid><startdate>20000701</startdate><enddate>20000701</enddate><creator>Brinkmeier, Heinrich</creator><creator>Aulkemeyer, Peter</creator><creator>Wollinsky, Kurt H.</creator><creator>Rüdel, Reinhardt</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20000701</creationdate><title>An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system</title><author>Brinkmeier, Heinrich ; Aulkemeyer, Peter ; Wollinsky, Kurt H. ; Rüdel, Reinhardt</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-a0a49dee16abb03dace6f3e9cf6532f63bd7d1c6c70626b0f832efad70986fc23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Central nervous system</topic><topic>Cerebrospinal fluid</topic><topic>Cerebrospinal Fluid - chemistry</topic><topic>Chromatography</topic><topic>Guillain-Barre Syndrome - cerebrospinal fluid</topic><topic>Humans</topic><topic>Inactivation</topic><topic>Infectious Diseases</topic><topic>Lesions</topic><topic>Metabolic Diseases</topic><topic>Molecular Medicine</topic><topic>Molecular weight</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - cerebrospinal fluid</topic><topic>Neurons - drug effects</topic><topic>Neurosciences</topic><topic>Oligopeptides - isolation & purification</topic><topic>Oligopeptides - pharmacology</topic><topic>Patients</topic><topic>pentapeptides</topic><topic>Peptides</topic><topic>Sequence Analysis, Protein</topic><topic>Sodium</topic><topic>sodium antagonists</topic><topic>Sodium Channel Blockers</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brinkmeier, Heinrich</creatorcontrib><creatorcontrib>Aulkemeyer, Peter</creatorcontrib><creatorcontrib>Wollinsky, Kurt H.</creatorcontrib><creatorcontrib>Rüdel, Reinhardt</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brinkmeier, Heinrich</au><au>Aulkemeyer, Peter</au><au>Wollinsky, Kurt H.</au><au>Rüdel, Reinhardt</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2000-07-01</date><risdate>2000</risdate><volume>6</volume><issue>7</issue><spage>808</spage><epage>811</epage><pages>808-811</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>Reversible blockade of sodium channels by endogenous substances has been claimed to account for the fast exacerbations and relapses commonly seen in demyelinating autoimmune diseases
2
,
3
,
4
. Evidence has been provided that in the cerebrospinal fluid of patients with multiple sclerosis
5
or Guillain-Barré syndrome
6
, a sodium-channel-blocking factor exists that has properties of local anesthetic agents
7
,
8
. This factor could contribute to the nerve conduction block and paresis seen in these disorders
9
,
10
,
11
. We describe here a previously unknown endogenous substance in human cerebrospinal fluid with distinct channel-blocking properties even at very low (0.00001 M) concentrations. The pentapeptide with the sequence Gln-Tyr-Asn-Ala-Asp exerted its blocking action by shifting the steady-state inactivation curve of the sodium channels to more-negative potentials, as most local anesthetics do. In the cerebrospinal fluid of healthy individuals, its concentration was about 3 μM, whereas in patients with multiple sclerosis and Guillain-Barré syndrome, it increased 300–1,400%. At these concentrations, the peptide's blocking efficacy was higher than that of 50 μM lidocaine. At a concentration of 10 μM, lidocaine is able to ‘unmask’ subclinical lesions in multiple sclerosis
12
; thus, the endogenous pentapeptide may well contribute to the fast changes of symptoms. Furthermore, it may become valuable as a marker of disease activity.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>10888931</pmid><doi>10.1038/77543</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1078-8956 |
| ispartof | Nature medicine, 2000-07, Vol.6 (7), p.808-811 |
| issn | 1078-8956 1546-170X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71219685 |
| source | MEDLINE; Nature; SpringerLink Journals - AutoHoldings |
| subjects | Autoimmune diseases Biomedical and Life Sciences Biomedicine Cancer Research Central nervous system Cerebrospinal fluid Cerebrospinal Fluid - chemistry Chromatography Guillain-Barre Syndrome - cerebrospinal fluid Humans Inactivation Infectious Diseases Lesions Metabolic Diseases Molecular Medicine Molecular weight Multiple sclerosis Multiple Sclerosis - cerebrospinal fluid Neurons - drug effects Neurosciences Oligopeptides - isolation & purification Oligopeptides - pharmacology Patients pentapeptides Peptides Sequence Analysis, Protein Sodium sodium antagonists Sodium Channel Blockers Tumor Cells, Cultured |
| title | An endogenous pentapeptide acting as a sodium channel blocker in inflammatory autoimmune disorders of the central nervous system |
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