A possible mechanism of repetitive firing of myelinated axon
A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented b...
Gespeichert in:
| Veröffentlicht in: | Pflügers Archiv 2009-07, Vol.458 (3), p.547-561 |
|---|---|
| 1. Verfasser: | |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 561 |
|---|---|
| container_issue | 3 |
| container_start_page | 547 |
| container_title | Pflügers Archiv |
| container_volume | 458 |
| creator | Dimitrov, Alexander G. |
| description | A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible. |
| doi_str_mv | 10.1007/s00424-009-0640-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67322993</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67322993</sourcerecordid><originalsourceid>FETCH-LOGICAL-c369t-2e5bae856f1d7c299eed1936385447fefdfa8aba72f0c231c345671eb4733ae53</originalsourceid><addsrcrecordid>eNp1kE1LAzEQhoMotlZ_gBdZPHhbnXxssgteSvELCl70HLK7E03ZL5Ot2H9vSgsFwdPA8Mw7Mw8hlxRuKYC6CwCCiRSgSEEKSPMjMqWCs5QB5cdkCsBpKpXMJ-QshBUAMJGzUzKhBYNMMTkl9_Nk6ENwZYNJi9Wn6Vxok94mHgcc3ei-MbHOu-5j22w32LjOjFgn5qfvzsmJNU3Ai32dkffHh7fFc7p8fXpZzJdpxWUxpgyz0mCeSUtrVbGiQKxpwSXPMyGURVtbk5vSKGahYpxWXGRSUSyF4txgxmfkZpc7-P5rjWHUrQsVNo3psF8HLRVnMZZH8PoPuOrXvou3aRafV1IUNEJ0B1U-fu7R6sG71viNpqC3XvXOq45e9darzuPM1T54XbZYHyb2IiPAdkAYtrLQHzb_n_oL_eOBzg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>200276491</pqid></control><display><type>article</type><title>A possible mechanism of repetitive firing of myelinated axon</title><source>MEDLINE</source><source>Springer Journals</source><creator>Dimitrov, Alexander G.</creator><creatorcontrib>Dimitrov, Alexander G.</creatorcontrib><description>A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-009-0640-8</identifier><identifier>PMID: 19205726</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Action Potentials - physiology ; Animals ; Biological Clocks - physiology ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Computer Simulation ; Human Physiology ; Humans ; Models, Neurological ; Molecular Medicine ; Nerve Fibers, Myelinated - physiology ; Neuroscience ; Neurosciences ; Receptors ; Sodium</subject><ispartof>Pflügers Archiv, 2009-07, Vol.458 (3), p.547-561</ispartof><rights>Springer-Verlag 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c369t-2e5bae856f1d7c299eed1936385447fefdfa8aba72f0c231c345671eb4733ae53</citedby><cites>FETCH-LOGICAL-c369t-2e5bae856f1d7c299eed1936385447fefdfa8aba72f0c231c345671eb4733ae53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00424-009-0640-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-009-0640-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19205726$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dimitrov, Alexander G.</creatorcontrib><title>A possible mechanism of repetitive firing of myelinated axon</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible.</description><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Biological Clocks - physiology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Computer Simulation</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Models, Neurological</subject><subject>Molecular Medicine</subject><subject>Nerve Fibers, Myelinated - physiology</subject><subject>Neuroscience</subject><subject>Neurosciences</subject><subject>Receptors</subject><subject>Sodium</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</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>eNp1kE1LAzEQhoMotlZ_gBdZPHhbnXxssgteSvELCl70HLK7E03ZL5Ot2H9vSgsFwdPA8Mw7Mw8hlxRuKYC6CwCCiRSgSEEKSPMjMqWCs5QB5cdkCsBpKpXMJ-QshBUAMJGzUzKhBYNMMTkl9_Nk6ENwZYNJi9Wn6Vxok94mHgcc3ei-MbHOu-5j22w32LjOjFgn5qfvzsmJNU3Ai32dkffHh7fFc7p8fXpZzJdpxWUxpgyz0mCeSUtrVbGiQKxpwSXPMyGURVtbk5vSKGahYpxWXGRSUSyF4txgxmfkZpc7-P5rjWHUrQsVNo3psF8HLRVnMZZH8PoPuOrXvou3aRafV1IUNEJ0B1U-fu7R6sG71viNpqC3XvXOq45e9darzuPM1T54XbZYHyb2IiPAdkAYtrLQHzb_n_oL_eOBzg</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Dimitrov, Alexander G.</creator><general>Springer-Verlag</general><general>Springer Nature 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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20090701</creationdate><title>A possible mechanism of repetitive firing of myelinated axon</title><author>Dimitrov, Alexander G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-2e5bae856f1d7c299eed1936385447fefdfa8aba72f0c231c345671eb4733ae53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Biological Clocks - physiology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Computer Simulation</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Models, Neurological</topic><topic>Molecular Medicine</topic><topic>Nerve Fibers, Myelinated - physiology</topic><topic>Neuroscience</topic><topic>Neurosciences</topic><topic>Receptors</topic><topic>Sodium</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dimitrov, Alexander G.</creatorcontrib><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>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>ProQuest 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>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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dimitrov, Alexander G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A possible mechanism of repetitive firing of myelinated axon</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>458</volume><issue>3</issue><spage>547</spage><epage>561</epage><pages>547-561</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>19205726</pmid><doi>10.1007/s00424-009-0640-8</doi><tpages>15</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0031-6768 |
| ispartof | Pflügers Archiv, 2009-07, Vol.458 (3), p.547-561 |
| issn | 0031-6768 1432-2013 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67322993 |
| source | MEDLINE; Springer Journals |
| subjects | Action Potentials - physiology Animals Biological Clocks - physiology Biomedical and Life Sciences Biomedicine Cell Biology Computer Simulation Human Physiology Humans Models, Neurological Molecular Medicine Nerve Fibers, Myelinated - physiology Neuroscience Neurosciences Receptors Sodium |
| title | A possible mechanism of repetitive firing of myelinated axon |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T18%3A39%3A23IST&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=A%20possible%20mechanism%20of%20repetitive%20firing%20of%20myelinated%20axon&rft.jtitle=Pfl%C3%BCgers%20Archiv&rft.au=Dimitrov,%20Alexander%20G.&rft.date=2009-07-01&rft.volume=458&rft.issue=3&rft.spage=547&rft.epage=561&rft.pages=547-561&rft.issn=0031-6768&rft.eissn=1432-2013&rft_id=info:doi/10.1007/s00424-009-0640-8&rft_dat=%3Cproquest_cross%3E67322993%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=200276491&rft_id=info:pmid/19205726&rfr_iscdi=true |